Prognostic and therapeutic methods for non-small cell lung cancer

Abstract

The present invention relates to prognostic and therapeutic methods for the treatment of non- small cell lung cancer (NSCLC) using expression levels of CD8+ T cell-associated genes. In particular, the invention provides methods for patient selection and treatment.

Description

[0001]PATENT Attorney Docket No.: 50474-320WO2 Genentech Docket No.: P38318-WO PROGNOSTIC AND THERAPEUTIC METHODS FOR NON-SMALL CELL LUNG CANCER SEQUENCE LISTING The instant application contains a Sequence Listing which has been submitted electronically in XML format and is hereby incorporated by reference in its entirety. Said XML copy, created on February 14, 2024, is named 50474-320WO2_Sequence_Listing_2_14_24 and is 6,606 bytes in size. FIELD OF THE INVENTION The present invention relates to prognostic and therapeutic methods for the treatment of non- small cell lung cancer (NSCLC) using expression levels of CD8+T cell-associated genes. In particular, the invention provides methods for patient selection and treatment. BACKGROUND Non-small cell lung cancer (NSCLC) is the predominant subtype of lung cancer, accounting for approximately 80%-85% of all cases. For advanced disease, the overall five-year survival rate is 2%-4%. Despite improvements in the first-line treatment of patients with advanced NSCLC that have resulted in longer survival times and reduced disease-related symptoms, nearly all patients experience disease progression. Programmed cell death-1 / programmed cell death ligand-1 (PD-1 / PD-L1) blockade is efficacious across a broad range of malignancies. However, not all patients benefit, and a significant fraction of initial responders eventually relapse. One approach to extend and expand the impact of cancer immunotherapy has been to target additional immune checkpoints. One such co-inhibitory checkpoint is TIGIT (T cell immunoreceptor with Ig and immunoreceptor tyrosine-based inhibitory motif (ITIM) domain). Thus, there is an unmet need in the field for robust prognostic methods that identify patients likely to benefit from a treatment comprising atezolizumab and / or tiragolumab for more effective management of the disease. SUMMARY OF THE INVENTION In one aspect, the invention provides a method of identifying an individual having a non-small cell lung cancer (NSCLC) who may benefit from a treatment comprising atezolizumab and tiragolumab, the method comprising detecting an expression level of one or more of CCL5, CXCR3, CCR7, and CXCR6 in a sample from the individual, wherein an expression level of one or more of CCL5, CXCR3, CCR7, and CXCR6 that is at or above a reference expression level of CCL5, CXCR3, CCR7, or CXCR6 identifies the individual as one who may benefit from a treatment comprising atezolizumab and tiragolumab. In another aspect, the invention provides a method for selecting a therapy for an individual having a NSCLC, the method comprising detecting an expression level of one or more of CCL5, CXCR3, CCR7, and CXCR6 in a sample from the individual, wherein an expression level of one or more of CCL5, CXCR3, CCR7, and CXCR6 that is at or above a reference expression level of CCL5, CXCR3, CCR7, or CXCR6 identifies the individual as one who may benefit from a treatment comprising atezolizumab and tiragolumab. PATENT Attorney Docket No.: 50474-320WO2 Genentech Docket No.: P38318-WO In some aspects, the individual has an expression level of one or more of CCL5, CXCR3, CCR7, and CXCR6 in the sample that is at or above a reference expression level of CCL5, CXCR3, CCR7, or CXCR6, and the method further comprises administering to the individual an effective amount of atezolizumab and tiragolumab. In another aspect, the invention provides a method of treating an individual having a NSCLC, the method comprising (a) detecting an expression level of one or more of CCL5, CXCR3, CCR7, and CXCR6 in a sample from the individual, wherein the expression level of one or more of CCL5, CXCR3, CCR7, and CXCR6 is at or above a reference expression level of CCL5, CXCR3, CCR7, or CXCR6 and thereby identifies the individual as one who may benefit from a treatment comprising atezolizumab and tiragolumab; and (b) administering an effective amount of atezolizumab and tiragolumab to the individual. In another aspect, the invention provides a method of treating an individual having a NSCLC, the method comprising administering atezolizumab and tiragolumab to the individual, wherein the individual has been determined to have an expression level of one or more of CCL5, CXCR3, CCR7, and CXCR6 that is at or above a reference expression level of CCL5, CXCR3, CCR7, or CXCR6, thereby identifying the individual as one who may benefit from a treatment comprising atezolizumab and tiragolumab. In some aspects, the benefit is a clinical response. In some aspects, the clinical response is a complete response (CR) or a partial response (PR). In some aspects, the individual has an expression level of one or more of CCL5, CXCR3, and CCR7 in the sample that is at or above a reference expression level of CCL5, CXCR3, or CCR7 and the benefit is an increase in overall survival (OS) hazard ratio (HR). In some aspects, the individual has an expression level of one or more of CCL5, CXCR3, and CXCR6 in the sample that is at or above a reference expression level of CCL5, CXCR3, or CXCR6 and the benefit is an increase in overall survival (OS). In some aspects, the reference expression level of CCL5, CXCR3, or CXCR6 is a pre-assigned expression level. In some aspects, the reference expression level of CCL5, CXCR3, or CXCR6 is an expression level in a reference population. In some aspects, the expression level in the reference population is the median expression level of CCL5, CXCR3, or CXCR6 in the reference population. In some aspects, the reference population is a population of individuals having the NSCLC. In another aspect, the invention provides a method of identifying an individual having a NSCLC who may benefit from a treatment comprising atezolizumab and tiragolumab, the method comprising detecting an expression level of each of CCL5, CXCR3, and CXCR6 in a sample from the individual and determining a gene signature score therefrom, wherein a gene signature score that is at or above a reference gene signature score identifies the individual as one who may benefit from a treatment comprising atezolizumab and tiragolumab. In another aspect, the invention provides a method for selecting a therapy for an individual having a NSCLC, the method comprising detecting an expression level of each of CCL5, CXCR3, and CXCR6 in a sample from the individual and determining a gene signature score therefrom, wherein a gene signature score that is at or above a reference gene signature score identifies the individual as one who may benefit from a treatment comprising atezolizumab and tiragolumab. PATENT Attorney Docket No.: 50474-320WO2 Genentech Docket No.: P38318-WO In some aspects, the individual has a gene signature score in the sample that is at or above a reference gene signature score, and the method further comprises administering to the individual an effective amount of atezolizumab and tiragolumab. In another aspect, the invention provides a method of treating an individual having a NSCLC, the method comprising (a) detecting an expression level of each of CCL5, CXCR3, and CXCR6 in a sample from the individual and determining a gene signature score therefrom, wherein the gene signature score is at or above a reference gene signature score and thereby identifies the individual as one who may benefit from a treatment comprising atezolizumab and tiragolumab; and (b) administering an effective amount of atezolizumab and tiragolumab to the individual. In another aspect, the invention provides a method of treating an individual having a NSCLC, the method comprising administering atezolizumab and tiragolumab to the individual, wherein the individual has been determined to have a gene signature score that is at or above a reference gene signature score, thereby identifying the individual as one who may benefit from a treatment comprising atezolizumab and tiragolumab, and wherein the gene signature score is based on the expression level of each of CCL5, CXCR3, and CXCR6 detected in a sample from the individual. In some aspects, the gene signature score is an average of the expression levels of CCL5, CXCR3, and CXCR6 in the sample from the individual. In some aspects, the method comprises further detecting the expression level of CCR7 in the sample from the individual. In some aspects, the gene signature score is an average of the expression levels of CCL5, CXCR3, CXCR6, and CCR7 in the sample from the individual. In some aspects, the expression level of CCR7 has been detected in the sample from the individual. In some aspects, the gene signature score is an average of the expression levels of CCL5, CXCR3, CXCR6, and CCR7 in the sample from the individual. In some aspects, the benefit is a clinical response. In some aspects, the clinical response is a CR or a PR. In some aspects, the benefit is an increase in OS HR. In some aspects, the benefit is an increase in OS. In some aspects, the reference gene signature score is a pre-assigned gene signature score. In some aspects, the reference gene signature score is a gene signature score in a reference population. In some aspects, the gene signature score in the reference population is the median gene signature score based on the expression level of each of CCL5, CXCR3, and CXCR6 in the reference population. In some aspects, the reference population is a population of individuals having the NSCLC. In another aspect, the invention provides a method of identifying an individual having a NSCLC who may benefit from a treatment comprising atezolizumab and tiragolumab, the method comprising: (a) detecting an expression level of each of STAT1, LEF1, IRGM, CCR7, SELL, RPS24, RPS27, GBP2, RPS29, RPS3A, RPS20, KLF2, RPLP1, RPL13, DAPL1, SMC6, RFLNB, and RPS4X in a sample from the individual and determining a Ccr7.2 gene signature score therefrom; (b) detecting an expression level of each of DAPL1, CCR7, SMC4, RGCC, MXD4, CD8A, TCF7, ITGAE, RGS10, ZNRF1, CHD3, CD52, DDIT4, LEF1, IZUMO1R, INPP4B, and RFLNB in a sample from the individual and determining a Ccr7.3 gene signature score therefrom; PATENT Attorney Docket No.: 50474-320WO2 Genentech Docket No.: P38318-WO (c) detecting an expression level of each of CXCR6, CKB, GIMAP5, ID2, LTB, FGL2, RAMP1, LYST, ASB2, IL2RB, CXCR3, SERINC3, INPP4B, ANXA1, XCL2, SOCS2, CD82, CD4, and GIMAP7 in a sample from the individual and determining a Cxcr3 gene signature score therefrom; (d) detecting an expression level of each of CCL5, ITGB1, BTG1, GZMK, LTB, IL7R, ZFP36L2, ITGA4, TXNIP, SLAMF6, HCST, ETS1, CXCR3, MS4A4A, DGKA, and YPEL3 in a sample from the individual and determining a Ccl5.1 gene signature score therefrom; (e) detecting an expression level of each of ISG15, IFIT1B, IFIT3, ISG20, IFI27L2, SAMHD1, ZBP1, SLFN5, IRF7, RTP4, USP18, PHF11, LGALS3BP, BST2, GBP2, IFITM3, STAT1, IFI16, and IFIH1 in a sample from the individual and determining an Ifit gene signature score therefrom; (f) detecting an expression level of each of HSP90AB1, PTMA, XCL2, ODC1, TNFRSF9, ITM2A, MYC, YBX3, HSPA5, GPX1, RPS12, TUBA1B, MCM6, TUBB, MCM3, TPI1, MCM5, DUT, and FTL in a sample from the individual and determining a Mitotic gene signature score therefrom; (g) detecting an expression level of each of HMGB2, TOP2A, MKI67, RRM2, PCLAF, TUBB, BIRC5, LMNB1, UBE2C, PTMA, STMN1, HMGN2, TUBA1B, LY6E, and DUT in a sample from the individual and determining a Cytotox.2 gene signature score therefrom; or (h) detecting an expression level of each of S100A6, NRN1, CXCR6, KLRC1, PDCD1, LGALS1, LAG3, ITGB1, ID2, LGALS3, NRGN, CST7, NKG7, S100A10, TNFRSF9, CD52, VIM, and IFITM2 in a sample from the individual and determining a Cytotox.4 gene signature score therefrom; wherein (i) a Ccr7.2, Ccr7.3, Cxcr3, Ccl5.1, Ifit, or Mitotic gene signature score that is at or above a reference gene signature score identifies the individual as one who may benefit from a treatment comprising atezolizumab and tiragolumab, and (ii) a Cytotox.2 or Cytotox.4 gene signature score that is below a reference gene signature score identifies the individual as one who may benefit from a treatment comprising atezolizumab and tiragolumab. In another aspect, the invention provides a method for selecting a therapy for an individual having a NSCLC, the method comprising: (a) detecting an expression level of each of STAT1, LEF1, IRGM, CCR7, SELL, RPS24, RPS27, GBP2, RPS29, RPS3A, RPS20, KLF2, RPLP1, RPL13, DAPL1, SMC6, RFLNB, and RPS4X in a sample from the individual and determining a Ccr7.2 gene signature score therefrom; (b) detecting an expression level of each of DAPL1, CCR7, SMC4, RGCC, MXD4, CD8A, TCF7, ITGAE, RGS10, ZNRF1, CHD3, CD52, DDIT4, LEF1, IZUMO1R, INPP4B, and RFLNB in a sample from the individual and determining a Ccr7.3 gene signature score therefrom; (c) detecting an expression level of each of CXCR6, CKB, GIMAP5, ID2, LTB, FGL2, RAMP1, LYST, ASB2, IL2RB, CXCR3, SERINC3, INPP4B, ANXA1, XCL2, SOCS2, CD82, CD4, and GIMAP7 in a sample from the individual and determining a Cxcr3 gene signature score therefrom; (d) detecting an expression level of each of CCL5, ITGB1, BTG1, GZMK, LTB, IL7R, ZFP36L2, ITGA4, TXNIP, SLAMF6, HCST, ETS1, CXCR3, MS4A4A, DGKA, and YPEL3 in a sample from the individual and determining a Ccl5.1 gene signature score therefrom; PATENT Attorney Docket No.: 50474-320WO2 Genentech Docket No.: P38318-WO (e) detecting an expression level of each of ISG15, IFIT1B, IFIT3, ISG20, IFI27L2, SAMHD1, ZBP1, SLFN5, IRF7, RTP4, USP18, PHF11, LGALS3BP, BST2, GBP2, IFITM3, STAT1, IFI16, and IFIH1 in a sample from the individual and determining an Ifit gene signature score therefrom; (f) detecting an expression level of each of HSP90AB1, PTMA, XCL2, ODC1, TNFRSF9, ITM2A, MYC, YBX3, HSPA5, GPX1, RPS12, TUBA1B, MCM6, TUBB, MCM3, TPI1, MCM5, DUT, and FTL in a sample from the individual and determining a Mitotic gene signature score therefrom; (g) detecting an expression level of each of HMGB2, TOP2A, MKI67, RRM2, PCLAF, TUBB, BIRC5, LMNB1, UBE2C, PTMA, STMN1, HMGN2, TUBA1B, LY6E, and DUT in a sample from the individual and determining a Cytotox.2 gene signature score therefrom; or (h) detecting an expression level of each of S100A6, NRN1, CXCR6, KLRC1, PDCD1, LGALS1, LAG3, ITGB1, ID2, LGALS3, NRGN, CST7, NKG7, S100A10, TNFRSF9, CD52, VIM, and IFITM2 in a sample from the individual and determining a Cytotox.4 gene signature score therefrom; wherein (i) a Ccr7.2, Ccr7.3, Cxcr3, Ccl5.1, Ifit, or Mitotic gene signature score that is at or above a reference gene signature score identifies the individual as one who may benefit from a treatment comprising atezolizumab and tiragolumab, and (ii) a Cytotox.2 or Cytotox.4 gene signature score that is below a reference gene signature score identifies the individual as one who may benefit from a treatment comprising atezolizumab and tiragolumab. In some aspects, the individual has (i) a Ccr7.2, Ccr7.3, Cxcr3, Ccl5.1, Ifit, or Mitotic gene signature score in the sample that is at or above a reference gene signature score or (ii) a Cytotox.2 or Cytotox.4 gene signature score that is below a reference gene signature score, and the method further comprises administering to the individual an effective amount of atezolizumab and tiragolumab. In another aspect, the invention provides a method of treating an individual having a NSCLC, the method comprising: (i) (a) detecting an expression level of each of STAT1, LEF1, IRGM, CCR7, SELL, RPS24, RPS27, GBP2, RPS29, RPS3A, RPS20, KLF2, RPLP1, RPL13, DAPL1, SMC6, RFLNB, and RPS4X in a sample from the individual and determining a Ccr7.2 gene signature score therefrom, wherein the gene signature score is at or above a reference gene signature score and thereby identifies the individual as one who may benefit from a treatment comprising atezolizumab and tiragolumab; (b) detecting an expression level of each of DAPL1, CCR7, SMC4, RGCC, MXD4, CD8A, TCF7, ITGAE, RGS10, ZNRF1, CHD3, CD52, DDIT4, LEF1, IZUMO1R, INPP4B, and RFLNB in a sample from the individual and determining a Ccr7.3 gene signature score therefrom, wherein the gene signature score is at or above a reference gene signature score and thereby identifies the individual as one who may benefit from a treatment comprising atezolizumab and tiragolumab; (c) detecting an expression level of each of CXCR6, CKB, GIMAP5, ID2, LTB, FGL2, RAMP1, LYST, ASB2, IL2RB, CXCR3, SERINC3, INPP4B, ANXA1, XCL2, SOCS2, CD82, CD4, and GIMAP7 in a sample from the individual and determining a Cxcr3 gene signature score therefrom, wherein the gene signature score is at or above a reference gene signature score and thereby identifies the individual as one who may benefit from a treatment comprising atezolizumab and tiragolumab; PATENT Attorney Docket No.: 50474-320WO2 Genentech Docket No.: P38318-WO (d) detecting an expression level of each of CCL5, ITGB1, BTG1, GZMK, LTB, IL7R, ZFP36L2, ITGA4, TXNIP, SLAMF6, HCST, ETS1, CXCR3, MS4A4A, DGKA, and YPEL3 in a sample from the individual and determining a Ccl5.1 gene signature score therefrom, wherein the gene signature score is at or above a reference gene signature score and thereby identifies the individual as one who may benefit from a treatment comprising atezolizumab and tiragolumab; (e) detecting an expression level of each of ISG15, IFIT1B, IFIT3, ISG20, IFI27L2, SAMHD1, ZBP1, SLFN5, IRF7, RTP4, USP18, PHF11, LGALS3BP, BST2, GBP2, IFITM3, STAT1, IFI16, and IFIH1 in a sample from the individual and determining an Ifit gene signature score therefrom, wherein the gene signature score is at or above a reference gene signature score and thereby identifies the individual as one who may benefit from a treatment comprising atezolizumab and tiragolumab; (f) detecting an expression level of each of HSP90AB1, PTMA, XCL2, ODC1, TNFRSF9, ITM2A, MYC, YBX3, HSPA5, GPX1, RPS12, TUBA1B, MCM6, TUBB, MCM3, TPI1, MCM5, DUT, and FTL in a sample from the individual and determining a Mitotic gene signature score therefrom, wherein the gene signature score is at or above a reference gene signature score and thereby identifies the individual as one who may benefit from a treatment comprising atezolizumab and tiragolumab; (g) detecting an expression level of each of HMGB2, TOP2A, MKI67, RRM2, PCLAF, TUBB, BIRC5, LMNB1, UBE2C, PTMA, STMN1, HMGN2, TUBA1B, LY6E, and DUT in a sample from the individual and determining a Cytotox.2 gene signature score therefrom, wherein the gene signature score is below a reference gene signature score and thereby identifies the individual as one who may benefit from a treatment comprising atezolizumab and tiragolumab; or (h) detecting an expression level of each of S100A6, NRN1, CXCR6, KLRC1, PDCD1, LGALS1, LAG3, ITGB1, ID2, LGALS3, NRGN, CST7, NKG7, S100A10, TNFRSF9, CD52, VIM, and IFITM2 in a sample from the individual and determining a Cytotox.4 gene signature score therefrom, wherein the gene signature score is below a reference gene signature score and thereby identifies the individual as one who may benefit from a treatment comprising atezolizumab and tiragolumab; and (ii) administering an effective amount of atezolizumab and tiragolumab to the individual. In another aspect, the invention provides a method of treating an individual having a NSCLC, the method comprising administering atezolizumab and tiragolumab to the individual, wherein the individual has been determined to have: (a) a Ccr7.2 gene signature score based on an expression level of each of STAT1, LEF1, IRGM, CCR7, SELL, RPS24, RPS27, GBP2, RPS29, RPS3A, RPS20, KLF2, RPLP1, RPL13, DAPL1, SMC6, RFLNB, and RPS4X in a sample from the individual that is at or above a reference Ccr7.2 gene signature score; (b) a Ccr7.3 gene signature based on an expression level of each of DAPL1, CCR7, SMC4, RGCC, MXD4, CD8A, TCF7, ITGAE, RGS10, ZNRF1, CHD3, CD52, DDIT4, LEF1, IZUMO1R, INPP4B, and RFLNB in a sample from the individual that is at or above a reference Ccr7.3 gene signature score; (c) a Cxcr3 gene signature score based on an expression level of each of CXCR6, CKB, GIMAP5, ID2, LTB, FGL2, RAMP1, LYST, ASB2, IL2RB, CXCR3, SERINC3, INPP4B, ANXA1, XCL2, SOCS2, CD82, CD4, and GIMAP7 in a sample from the individual that is at or above a reference Cxcr3 gene signature score; PATENT Attorney Docket No.: 50474-320WO2 Genentech Docket No.: P38318-WO (d) a Ccl5.1 gene signature score based on an expression level of each of CCL5, ITGB1, BTG1, GZMK, LTB, IL7R, ZFP36L2, ITGA4, TXNIP, SLAMF6, HCST, ETS1, CXCR3, MS4A4A, DGKA, and YPEL3 in a sample from the individual that is at or above a reference Ccl5.1 gene signature score; (e) an Ifit gene signature score based on an expression level of each of ISG15, IFIT1B, IFIT3, ISG20, IFI27L2, SAMHD1, ZBP1, SLFN5, IRF7, RTP4, USP18, PHF11, LGALS3BP, BST2, GBP2, IFITM3, STAT1, IFI16, and IFIH1 in a sample from the individual that is at or above a reference Ifit gene signature score; (f) a Mitotic gene signature score based on an expression level of each of HSP90AB1, PTMA, XCL2, ODC1, TNFRSF9, ITM2A, MYC, YBX3, HSPA5, GPX1, RPS12, TUBA1B, MCM6, TUBB, MCM3, TPI1, MCM5, DUT, and FTL in a sample from the individual that is at or above a reference Mitotic gene signature score; (g) a Cytotox.2 gene signature score based on an expression level of each of HMGB2, TOP2A, MKI67, RRM2, PCLAF, TUBB, BIRC5, LMNB1, UBE2C, PTMA, STMN1, HMGN2, TUBA1B, LY6E, and DUT in a sample from the individual that is below a reference Cytotox.2 gene signature score; or (h) a Cytotox.4 gene signature score based on an expression level of each of S100A6, NRN1, CXCR6, KLRC1, PDCD1, LGALS1, LAG3, ITGB1, ID2, LGALS3, NRGN, CST7, NKG7, S100A10, TNFRSF9, CD52, VIM, and IFITM2 in a sample from the individual that is below a reference Cytotox.4 gene signature score; thereby identifying the individual as one who may benefit from a treatment comprising atezolizumab and tiragolumab. In some aspects, the gene signature score is an average of the expression levels of the members of the gene signature in the sample from the individual. In some aspects, the individual has a Ccr7.3, Cxcr3, or Ccl5.1 gene signature score in the sample that is at or above a reference gene signature score and the benefit is a clinical response. In some aspects, the clinical response is a CR or a PR. In some aspects, the individual has (i) a Ccr7.2, Cxcr3, Ifit, or Mitotic gene signature score in the sample that is at or above a reference gene signature score or (ii) a Cytotox.2 or Cytotox.4 gene signature score that is below a reference gene signature score and the benefit is an increase in OS HR. In some aspects, the individual has a Ccr7.2, Ccr7.3, or Cxcr3 gene signature score in the sample that is at or above a reference gene signature score and the benefit is an increase in OS. In some aspects, the reference gene signature score is a pre-assigned gene signature score. In some aspects, the reference gene signature score is a gene signature score in a reference population. In some aspects, the gene signature score in the reference population is the median Ccr7.2, Ccr7.3, Cxcr3, Ccl5.1, Ifit, Mitotic, Cytotox.2, or Cytotox.4 gene signature score in the reference population. In some aspects, the reference population is a population of individuals having the NSCLC. In another aspect, the invention provides a method of identifying an individual having a NSCLC who may benefit from a treatment comprising atezolizumab, the method comprising detecting an expression level of each of CCL5, CXCR3, and CXCR6 in a sample from the individual and determining a gene signature score therefrom, wherein a gene signature score that is at or above a reference gene PATENT Attorney Docket No.: 50474-320WO2 Genentech Docket No.: P38318-WO signature score identifies the individual as one who may benefit from a treatment comprising atezolizumab. In another aspect, the invention provides a method for selecting a therapy for an individual having a NSCLC, the method comprising detecting an expression level of each of CCL5, CXCR3, and CXCR6 in a sample from the individual and determining a gene signature score therefrom, wherein a gene signature score that is at or above a reference gene signature score identifies the individual as one who may benefit from a treatment comprising atezolizumab. In some aspects, the individual has a gene signature score in the sample that is at or above a reference gene signature score, and the method further comprises administering to the individual an effective amount of atezolizumab. In another aspect, the invention provides a method of treating an individual having a NSCLC, the method comprising (a) detecting an expression level of each of CCL5, CXCR3, and CXCR6 in a sample from the individual and determining a gene signature score therefrom, wherein the gene signature score is at or above a reference gene signature score and thereby identifies the individual as one who may benefit from a treatment comprising atezolizumab; and (b) administering an effective amount of atezolizumab to the individual. In another aspect, the invention provides a method of treating an individual having a NSCLC, the method comprising administering atezolizumab to the individual, wherein the individual has been determined to have a gene signature score that is at or above a reference gene signature score, thereby identifying the individual as one who may benefit from a treatment comprising atezolizumab, and wherein the gene signature score is based on the expression level of each of CCL5, CXCR3, and CXCR6 detected in a sample from the individual. In some aspects, the gene signature score is an average of the expression levels of CCL5, CXCR3, and CXCR6 in the sample from the individual. In some aspects, the method comprises further detecting the expression level of CCR7 in the sample from the individual. In some aspects, the gene signature score is an average of the expression levels of CCL5, CXCR3, CXCR6, and CCR7 in the sample from the individual. In some aspects, the expression level of CCR7 has been detected in the sample from the individual. In some aspects, the gene signature score is an average of the expression levels of CCL5, CXCR3, CXCR6, and CCR7 in the sample from the individual. In some aspects, the benefit is an increase in progression-free survival (PFS) or OS. In some aspects, the reference gene signature score is a pre-assigned gene signature score. In some aspects, the reference gene signature score is a gene signature score in a reference population. In some aspects, the gene signature score in the reference population is the median gene signature score based on the expression level of each of CCL5, CXCR3, and CXCR6 in the reference population. In some aspects, the reference population is a population of individuals having the NSCLC. In some aspects, the treatment comprising atezolizumab is atezolizumab monotherapy. In another aspect, the invention provides use of atezolizumab and / or tiragolumab in the manufacture of a medicament for the treatment of an individual having a NSCLC, wherein the individual has been determined to have an expression level of one or more of CCL5, CXCR3, CCR7, and CXCR6 in PATENT Attorney Docket No.: 50474-320WO2 Genentech Docket No.: P38318-WO a sample from the individual that is at or above a reference expression level of CCL5, CXCR3, CCR7, or CXCR6, thereby identifying the individual as one who may benefit from a treatment comprising atezolizumab and tiragolumab. In some aspects, the benefit is a clinical response. In some aspects, the clinical response is a complete response (CR) or a partial response (PR). In some aspects, the individual has been determined to have an expression level of one or more of CCL5, CXCR3, and CCR7 in the sample that is at or above a reference expression level of CCL5, CXCR3, or CCR7 and the benefit is an increase in overall survival (OS) hazard ratio (HR). In some aspects, the individual has been determined to have an expression level of one or more of CCL5, CXCR3, and CXCR6 in the sample that is at or above a reference expression level of CCL5, CXCR3, or CXCR6 and the benefit is an increase in overall survival (OS). In some aspects, the reference expression level of CCL5, CXCR3, or CXCR6 is a pre-assigned expression level. In some aspects, the reference expression level of CCL5, CXCR3, or CXCR6 is an expression level in a reference population. In some aspects, the expression level in the reference population is the median expression level of CCL5, CXCR3, or CXCR6 in the reference population. In some aspects, the reference population is a population of individuals having the NSCLC. In another aspect, the invention provides use of atezolizumab and / or tiragolumab in the manufacture of a medicament for the treatment of an individual having a NSCLC, wherein the individual has been determined to have a gene signature score that is at or above a reference gene signature score, thereby identifying the individual as one who may benefit from a treatment comprising atezolizumab and tiragolumab, wherein the gene signature score is based on the expression level of each of CCL5, CXCR3, and CXCR6 detected in a sample from the individual. In some aspects, the gene signature score is an average of the expression levels of CCL5, CXCR3, and CXCR6 in the sample from the individual. In some aspects, the expression level of CCR7 has been detected in the sample from the individual. In some aspects, the gene signature score is an average of the expression levels of CCL5, CXCR3, CXCR6, and CCR7 in the sample from the individual. In some aspects, the benefit is a clinical response. In some aspects, the clinical response is a CR or a PR. In some aspects, the benefit is an increase in OS HR. In some aspects, the benefit is an increase in OS. In some aspects, the reference gene signature score is a pre-assigned gene signature score. In some aspects, the reference gene signature score is a gene signature score in a reference population. In some aspects, the gene signature score in the reference population is the median gene signature score based on the expression level of each of CCL5, CXCR3, and CXCR6 in the reference population. In some aspects, the reference population is a population of individuals having the NSCLC. In another aspect, the invention provides use of atezolizumab and / or tiragolumab in the manufacture of a medicament for the treatment of an individual having a NSCLC, wherein the individual has been determined to have: PATENT Attorney Docket No.: 50474-320WO2 Genentech Docket No.: P38318-WO (i) (a) a Ccr7.2 gene signature score that is at or above a reference gene signature score, thereby identifying the individual as one who may benefit from a treatment comprising atezolizumab and tiragolumab, wherein the gene signature score is based on the expression level of each of STAT1, LEF1, IRGM, CCR7, SELL, RPS24, RPS27, GBP2, RPS29, RPS3A, RPS20, KLF2, RPLP1, RPL13, DAPL1, SMC6, RFLNB, and RPS4X detected in a sample from the individual; (b) a Ccr7.3 gene signature score that is at or above a reference gene signature score, thereby identifying the individual as one who may benefit from a treatment comprising atezolizumab and tiragolumab, wherein the gene signature score is based on the expression level of each of DAPL1, CCR7, SMC4, RGCC, MXD4, CD8A, TCF7, ITGAE, RGS10, ZNRF1, CHD3, CD52, DDIT4, LEF1, IZUMO1R, INPP4B, and RFLNB detected in a sample from the individual; (c) a Cxcr3 gene signature score that is at or above a reference gene signature score, thereby identifying the individual as one who may benefit from a treatment comprising atezolizumab and tiragolumab, wherein the gene signature score is based on the expression level of each of CXCR6, CKB, GIMAP5, ID2, LTB, FGL2, RAMP1, LYST, ASB2, IL2RB, CXCR3, SERINC3, INPP4B, ANXA1, XCL2, SOCS2, CD82, CD4, and GIMAP7 detected in a sample from the individual; (d) a Ccl5.1 gene signature score that is at or above a reference gene signature score, thereby identifying the individual as one who may benefit from a treatment comprising atezolizumab and tiragolumab, wherein the gene signature score is based on the expression level of each of CCL5, ITGB1, BTG1, GZMK, LTB, IL7R, ZFP36L2, ITGA4, TXNIP, SLAMF6, HCST, ETS1, CXCR3, MS4A4A, DGKA, and YPEL3 detected in a sample from the individual; (e) an Ifit gene signature score that is at or above a reference gene signature score, thereby identifying the individual as one who may benefit from a treatment comprising atezolizumab and tiragolumab, wherein the gene signature score is based on the expression level of each of ISG15, IFIT1B, IFIT3, ISG20, IFI27L2, SAMHD1, ZBP1, SLFN5, IRF7, RTP4, USP18, PHF11, LGALS3BP, BST2, GBP2, IFITM3, STAT1, IFI16, and IFIH1 detected in a sample from the individual; (f) a Mitotic gene signature score that is at or above a reference gene signature score, thereby identifying the individual as one who may benefit from a treatment comprising atezolizumab and tiragolumab, wherein the gene signature score is based on the expression level of each of HSP90AB1, PTMA, XCL2, ODC1, TNFRSF9, ITM2A, MYC, YBX3, HSPA5, GPX1, RPS12, TUBA1B, MCM6, TUBB, MCM3, TPI1, MCM5, DUT, and FTL detected in a sample from the individual; (g) a Cytotox.2 gene signature score that is below a reference gene signature score, thereby identifying the individual as one who may benefit from a treatment comprising atezolizumab and tiragolumab, wherein the gene signature score is based on the expression level of each of HMGB2, TOP2A, MKI67, RRM2, PCLAF, TUBB, BIRC5, LMNB1, UBE2C, PTMA, STMN1, HMGN2, TUBA1B, LY6E, and DUT detected in a sample from the individual; or (h) a Cytotox.4 gene signature score that is below a reference gene signature score, thereby identifying the individual as one who may benefit from a treatment comprising atezolizumab and tiragolumab, wherein the gene signature score is based on the expression level of each of S100A6, PATENT Attorney Docket No.: 50474-320WO2 Genentech Docket No.: P38318-WO NRN1, CXCR6, KLRC1, PDCD1, LGALS1, LAG3, ITGB1, ID2, LGALS3, NRGN, CST7, NKG7, S100A10, TNFRSF9, CD52, VIM, and IFITM2 detected in a sample from the individual. In some aspects, the gene signature score is an average of the expression levels of the members of the gene signature in the sample from the individual. In some aspects, the individual has been determined to have a Ccr7.3, Cxcr3, or Ccl5.1 gene signature score in the sample that is at or above a reference gene signature score and the benefit is a clinical response. In some aspects, the clinical response is a CR or a PR. In some aspects, the individual has been determined to have (i) a Ccr7.2, Cxcr3, Ifit, or Mitotic gene signature score in the sample that is at or above a reference gene signature score or (ii) a Cytotox.2 or Cytotox.4 gene signature score that is below a reference gene signature score and the benefit is an increase in OS HR. In some aspects, the individual has been determined to have a Ccr7.2, Ccr7.3, or Cxcr3 gene signature score in the sample that is at or above a reference gene signature score and the benefit is an increase in OS. In some aspects, the reference gene signature score is a pre-assigned gene signature score. In some aspects, the reference gene signature score is a gene signature score in a reference population. In some aspects, the gene signature score in the reference population is the median Ccr7.2, Ccr7.3, Cxcr3, Ccl5.1, Ifit, Mitotic, Cytotox.2, or Cytotox.4 gene signature score in the reference population. In some aspects, the reference population is a population of individuals having the NSCLC. In another aspect, the invention provides use of atezolizumab in the manufacture of a medicament for the treatment of an individual having a NSCLC, wherein the individual has been determined to have a gene signature score that is at or above a reference gene signature score, thereby identifying the individual as one who may benefit from a treatment comprising atezolizumab, wherein the gene signature score is based on the expression level of each of CCL5, CXCR3, and CXCR6 detected in a sample from the individual. In some aspects, the gene signature score is an average of the expression levels of CCL5, CXCR3, and CXCR6 in the sample from the individual. In some aspects, the expression level of CCR7 has been detected in the sample from the individual. In some aspects, the gene signature score is an average of the expression levels of CCL5, CXCR3, CXCR6, and CCR7 in the sample from the individual. In some aspects, the benefit is an increase in progression-free survival (PFS) or OS. In some aspects, the reference gene signature score is a pre-assigned gene signature score. In some aspects, the reference gene signature score is a gene signature score in a reference population. In some aspects, the gene signature score in the reference population is the median gene signature score based on the expression level of each of CCL5, CXCR3, and CXCR6 in the reference population. In some aspects, the reference population is a population of individuals having the NSCLC. In some aspects, the treatment comprising atezolizumab is atezolizumab monotherapy. In another aspect, the invention provides atezolizumab and / or tiragolumab for use in treating an individual having a NSCLC, wherein the individual has been determined to have an expression level of one or more of CCL5, CXCR3, CCR7, and CXCR6 in a sample from the individual that is at or above a PATENT Attorney Docket No.: 50474-320WO2 Genentech Docket No.: P38318-WO reference expression level of CCL5, CXCR3, CCR7, or CXCR6, thereby identifying the individual as one who may benefit from a treatment comprising atezolizumab and tiragolumab. In some aspects, the benefit is a clinical response. In some aspects, the clinical response is a complete response (CR) or a partial response (PR). In some aspects, the individual has been determined to have an expression level of one or more of CCL5, CXCR3, and CCR7 in the sample that is at or above a reference expression level of CCL5, CXCR3, or CCR7 and the benefit is an increase in overall survival (OS) hazard ratio (HR). In some aspects, the individual has been determined to have an expression level of one or more of CCL5, CXCR3, and CXCR6 in the sample that is at or above a reference expression level of CCL5, CXCR3, or CXCR6 and the benefit is an increase in overall survival (OS). In some aspects, the reference expression level of CCL5, CXCR3, or CXCR6 is a pre-assigned expression level. In some aspects, the reference expression level of CCL5, CXCR3, or CXCR6 is an expression level in a reference population. In some aspects, the expression level in the reference population is the median expression level of CCL5, CXCR3, or CXCR6 in the reference population. In some aspects, the reference population is a population of individuals having the NSCLC. In another aspect, the invention provides atezolizumab and / or tiragolumab for use in treating an individual having a NSCLC, wherein the individual has been determined to have a gene signature score that is at or above a reference gene signature score, thereby identifying the individual as one who may benefit from a treatment comprising atezolizumab and tiragolumab, wherein the gene signature score is based on the expression level of each of CCL5, CXCR3, and CXCR6 detected in a sample from the individual. In some aspects, the gene signature score is an average of the expression levels of CCL5, CXCR3, and CXCR6 in the sample from the individual. In some aspects, the expression level of CCR7 has been detected in the sample from the individual. In some aspects, the gene signature score is an average of the expression levels of CCL5, CXCR3, CXCR6, and CCR7 in the sample from the individual. In some aspects, the benefit is a clinical response. In some aspects, the clinical response is a CR or a PR. In some aspects, the benefit is an increase in OS HR. In some aspects, the benefit is an increase in OS. In some aspects, the reference gene signature score is a pre-assigned gene signature score. In some aspects, the reference gene signature score is a gene signature score in a reference population. In some aspects, the gene signature score in the reference population is the median gene signature score based on the expression level of each of CCL5, CXCR3, and CXCR6 in the reference population. In some aspects, the reference population is a population of individuals having the NSCLC. In another aspect, the invention provides atezolizumab and / or tiragolumab for use in treating an individual having a NSCLC, wherein the individual has been determined to have: PATENT Attorney Docket No.: 50474-320WO2 Genentech Docket No.: P38318-WO (i) (a) a Ccr7.2 gene signature score that is at or above a reference gene signature score, thereby identifying the individual as one who may benefit from a treatment comprising atezolizumab and tiragolumab, wherein the gene signature score is based on the expression level of each of STAT1, LEF1, IRGM, CCR7, SELL, RPS24, RPS27, GBP2, RPS29, RPS3A, RPS20, KLF2, RPLP1, RPL13, DAPL1, SMC6, RFLNB, and RPS4X detected in a sample from the individual; (b) a Ccr7.3 gene signature score that is at or above a reference gene signature score, thereby identifying the individual as one who may benefit from a treatment comprising atezolizumab and tiragolumab, wherein the gene signature score is based on the expression level of each of DAPL1, CCR7, SMC4, RGCC, MXD4, CD8A, TCF7, ITGAE, RGS10, ZNRF1, CHD3, CD52, DDIT4, LEF1, IZUMO1R, INPP4B, and RFLNB detected in a sample from the individual; (c) a Cxcr3 gene signature score that is at or above a reference gene signature score, thereby identifying the individual as one who may benefit from a treatment comprising atezolizumab and tiragolumab, wherein the gene signature score is based on the expression level of each of CXCR6, CKB, GIMAP5, ID2, LTB, FGL2, RAMP1, LYST, ASB2, IL2RB, CXCR3, SERINC3, INPP4B, ANXA1, XCL2, SOCS2, CD82, CD4, and GIMAP7 detected in a sample from the individual; (d) a Ccl5.1 gene signature score that is at or above a reference gene signature score, thereby identifying the individual as one who may benefit from a treatment comprising atezolizumab and tiragolumab, wherein the gene signature score is based on the expression level of each of CCL5, ITGB1, BTG1, GZMK, LTB, IL7R, ZFP36L2, ITGA4, TXNIP, SLAMF6, HCST, ETS1, CXCR3, MS4A4A, DGKA, and YPEL3 detected in a sample from the individual; (e) an Ifit gene signature score that is at or above a reference gene signature score, thereby identifying the individual as one who may benefit from a treatment comprising atezolizumab and tiragolumab, wherein the gene signature score is based on the expression level of each of ISG15, IFIT1B, IFIT3, ISG20, IFI27L2, SAMHD1, ZBP1, SLFN5, IRF7, RTP4, USP18, PHF11, LGALS3BP, BST2, GBP2, IFITM3, STAT1, IFI16, and IFIH1 detected in a sample from the individual; (f) a Mitotic gene signature score that is at or above a reference gene signature score, thereby identifying the individual as one who may benefit from a treatment comprising atezolizumab and tiragolumab, wherein the gene signature score is based on the expression level of each of HSP90AB1, PTMA, XCL2, ODC1, TNFRSF9, ITM2A, MYC, YBX3, HSPA5, GPX1, RPS12, TUBA1B, MCM6, TUBB, MCM3, TPI1, MCM5, DUT, and FTL detected in a sample from the individual; (g) a Cytotox.2 gene signature score that is below a reference gene signature score, thereby identifying the individual as one who may benefit from a treatment comprising atezolizumab and tiragolumab, wherein the gene signature score is based on the expression level of each of HMGB2, TOP2A, MKI67, RRM2, PCLAF, TUBB, BIRC5, LMNB1, UBE2C, PTMA, STMN1, HMGN2, TUBA1B, LY6E, and DUT detected in a sample from the individual; or (h) a Cytotox.4 gene signature score that is below a reference gene signature score, thereby identifying the individual as one who may benefit from a treatment comprising atezolizumab and tiragolumab, wherein the gene signature score is based on the expression level of each of S100A6, PATENT Attorney Docket No.: 50474-320WO2 Genentech Docket No.: P38318-WO NRN1, CXCR6, KLRC1, PDCD1, LGALS1, LAG3, ITGB1, ID2, LGALS3, NRGN, CST7, NKG7, S100A10, TNFRSF9, CD52, VIM, and IFITM2 detected in a sample from the individual. In some aspects, the gene signature score is an average of the expression levels of the members of the gene signature in the sample from the individual. In some aspects, the individual has been determined to have a Ccr7.3, Cxcr3, or Ccl5.1 gene signature score in the sample that is at or above a reference gene signature score and the benefit is a clinical response. In some aspects, the clinical response is a CR or a PR. In some aspects, the individual has been determined to have (i) a Ccr7.2, Cxcr3, Ifit, or Mitotic gene signature score in the sample that is at or above a reference gene signature score or (ii) a Cytotox.2 or Cytotox.4 gene signature score that is below a reference gene signature score and the benefit is an increase in OS HR. In some aspects, the individual has been determined to have a Ccr7.2, Ccr7.3, or Cxcr3 gene signature score in the sample that is at or above a reference gene signature score and the benefit is an increase in OS. In some aspects, the reference gene signature score is a pre-assigned gene signature score. In some aspects, the reference gene signature score is a gene signature score in a reference population. In some aspects, the gene signature score in the reference population is the median Ccr7.2, Ccr7.3, Cxcr3, Ccl5.1, Ifit, Mitotic, Cytotox.2, or Cytotox.4 gene signature score in the reference population. In some aspects, the reference population is a population of individuals having the NSCLC. In another aspect, the invention provides atezolizumab for use in treating an individual having a NSCLC, wherein the individual has been determined to have a gene signature score that is at or above a reference gene signature score, thereby identifying the individual as one who may benefit from a treatment comprising atezolizumab, wherein the gene signature score is based on the expression level of each of CCL5, CXCR3, and CXCR6 detected in a sample from the individual. In some aspects, the gene signature score is an average of the expression levels of CCL5, CXCR3, and CXCR6 in the sample from the individual. In some aspects, the expression level of CCR7 has been detected in the sample from the individual. In some aspects, the gene signature score is an average of the expression levels of CCL5, CXCR3, CXCR6, and CCR7 in the sample from the individual. In some aspects, the benefit is an increase in progression-free survival (PFS) or OS. In some aspects, the reference gene signature score is a pre-assigned gene signature score. In some aspects, the reference gene signature score is a gene signature score in a reference population. In some aspects, the gene signature score in the reference population is the median gene signature score based on the expression level of each of CCL5, CXCR3, and CXCR6 in the reference population. In some aspects, the reference population is a population of individuals having the NSCLC. In some aspects, the treatment comprising atezolizumab is atezolizumab monotherapy. In some aspects, the expression level is a nucleic acid expression level or a protein expression level. PATENT Attorney Docket No.: 50474-320WO2 Genentech Docket No.: P38318-WO In some aspects, the expression level is a nucleic acid expression level. In some aspects, the nucleic acid expression level is determined by RNA-seq, RT-qPCR, qPCR, multiplex qPCR or RT-qPCR, microarray analysis, SAGE, MassARRAY technique, ISH, or a combination thereof. In some aspects, the nucleic acid expression level is an mRNA expression level. In some aspects, the mRNA expression level is determined by RNA-seq. In some aspects, the expression level is a protein expression level. In some aspects, the protein expression level is determined by mass spectrometry. In some aspects, the sample is obtained from the individual prior to treatment with atezolizumab and / or tiragolumab. In some aspects, the sample is a tissue sample, a tumor sample, a blood sample, a plasma sample, a serum sample, or a combination thereof. In some aspects, the sample is a tissue sample. In some aspects, the tissue sample is a tumor tissue sample. In some aspects, the tumor tissue sample is a biopsy. In some aspects, the tissue sample is a tumor draining lymph node (dLN) sample. In some aspects, the sample is a blood sample. In some aspects, the sample is an archival sample, a fresh sample, or a frozen sample. In some aspects, the individual has a PD-L1-positive NSCLC. In some aspects, the PD-L1- positive NSCLC has been determined to have a PD-L1-positive tumor cell fraction by an immunohistochemical (IHC) assay. In some aspects, the PD-L1-positive tumor cell fraction is determined by positive staining with an anti-PD-L1 antibody, wherein the anti-PD-L1 antibody is SP263, 22C3, SP142, or 28-8. In some aspects, the individual is a human. In some aspects, the individual has not previously been treated for NSCLC. BRIEF DESCRIPTION OF THE DRAWINGS FIG.1A is a set of graphs showing tumor volume (mm3) (log2scale) over time in BALB / c mice that were inoculated subcutaneously with syngeneic CT26 tumor cells and treated with an isotype control, anti-PD-L1, anti-TIGIT, or the combination of anti-PD-L1 and anti-TIGIT antibodies, with or without FTY720, an agent that blocks T cell egress from tumor draining lymph nodes (dLN). Grouped analysis (left panel) and growth curves for each individual animal (n = 10 per group) (right panels) are shown. Tumor growth efficacy study is representative of three independent experiments. FIG.1B is a set of bar graphs showing the frequency of CD8+T cells with positive staining for the gp70-specific tetramer in dLN (left panel); the number of CD8+T cells with positive staining for the gp70- specific tetramer in blood (right panel); and the frequency of CD8+T cells with positive staining for the gp70-specific tetramer in tumor (right panel) in BALB / c CT26 tumor model mice treated with an isotype control, anti-PD-L1, anti-TIGIT, and / or FTY720. p-values are indicated where differences between two groups were determined by two-way unpaired Student’s t-test to be statistically significant. FIG.1C is a bar graph showing quantitation of CD8+T cells producing IFN-g and TNF-a as a percentage of total CD8+tumor-infiltrating lymphocytes (TILs) in BALB / c CT26 tumor model mice treated with an isotype control, anti-PD-L1, anti-TIGIT, and / or FTY720. Pharmacodynamic data are PATENT Attorney Docket No.: 50474-320WO2 Genentech Docket No.: P38318-WO representative of three independent experiments (n = 5 per group). p-values are indicated where differences between two groups were determined by two-way unpaired Student’s t-test to be statistically significant. FIG.1D is a set of graphs showing tumor volume (mm3) (log2 scale) over time in BALB / c mice that were inoculated subcutaneously with syngeneic CT26 tumor cells, treated with an isotype control or the combination of anti-PD-L1 and anti-TIGIT antibodies, and treated with FTY720 at day 0, one day prior to initiation of therapy, or on day 7 after one week of therapy (delayed FTY720). Grouped analysis (left panel) and growth curves for each individual animal (n = 10 per group) (right panel) are shown. Tumor growth efficacy study is representative of three independent experiments. FIG.2A is a Uniform Manifold Approximation and Projection (UMAP) showing 174,514 CD8+T cells isolated from tumor, dLN, and blood of CT26 tumor model mice shaded by cluster. FIG.2B is a heatmap showing the relative average expression of selected marker genes associated with CD8+T cell phenotype, function, or differentiation state in each cluster identified in the UMAP shown in Fig.2A. FIG.2C is a set of stacked bar graphs of CD8+T cell cluster composition in lymph nodes and blood under the indicated treatment condition. In each stacked bar, an open bar denotes singletons, a solid bar denotes numbers for clones with less than 100 cells, and a hatched bar denotes numbers for clones with 100 or more cells. FIG.2D is a set of stacked bar graphs of CD8+T cell cluster composition in blood (Day 7) and tumor under the indicated treatment condition. In each stacked bar, an open bar denotes singletons, a solid bar denotes numbers for clones with less than 100 cells, and a hatched bar denotes numbers for clones with 100 or more cells. FIG.3A is an image showing relative clone sizes projected on the CD8+T cell UMAP shown in Fig.2A. Clonal diversity was determined by T cell receptor sequencing (TCR-seq). FIG.3B is an image showing antibody-derived tag (ADT) counts measured from cellular indexing of transcriptomes and epitopes (CITE-seq) projected on the CD8+T cell UMAP shown in Fig.2A. FIG.3C is an image showing the specificity of clones for gp70 subdivided by high (≥ 100) or low (< 100) ADT count projected on the CD8+T cell UMAP shown in Fig.2A and a stacked bar graph showing the fraction of cells in each cluster that are gp70+, gp70-, and have a high (≥ 100) or low (< 100) ADT count. FIG.3D is a set of scatterplots showing primary clusters of each individual clonotype in dLN (upper panels) or tumor (lower panels). Shade of circles denote cluster designation. Size of circles is representative of clonotype numbers detected in blood at day 7. FIG.3E is a set of scatterplots showing gp70 specificity and ADT count for individual clones. FIG.3F is a set of stacked bar graphs showing the cluster composition of the top 50 largest clones in tumor with matching clonotypes, based on identical TCR usage, in dLN and blood, in absolute numbers. Cluster identity is indicated by shade. FIG.4A is a set of UMAPs showing a cluster co-occurrence analysis in dLN (lymph), blood, and tumor samples from CT26 tumor model mice treated with a control anti-gp120 treatment. Lines within UMAPs denote co-occurrence between different clusters within the indicated tissue. Lines between PATENT Attorney Docket No.: 50474-320WO2 Genentech Docket No.: P38318-WO UMAPs denote co-occurrence between the same cluster in different tissues. Thickness of line denotes relative strength of co-occurrence, with thickest lines indicating strongest co-occurrence. For lines between tissues, shade of the line indicates the cluster. FIG.4B is a set of UMAPs showing a cluster co-occurrence analysis in dLN (lymph), blood, and tumor samples from CT26 tumor model mice treated with an anti-PD-L1 antibody. FIG.4C is a set of UMAPs showing a cluster co-occurrence analysis in dLN (lymph), blood, and tumor samples from CT26 tumor model mice treated with an anti-TIGIT antibody. FIG.4D is a set of UMAPs showing a cluster co-occurrence analysis in dLN (lymph), blood, and tumor samples from CT26 tumor model mice treated with an anti-TIGIT antibody and an anti-PD-L1 antibody. FIG.4E is a set of UMAPs showing a cluster co-occurrence analysis in dLN (lymph), blood, and tumor samples from CT26 tumor model mice treated with an anti-TIGIT antibody, an anti-PD-L1 antibody, and FTY720. FIG.5A is a plot showing the proportion of gp70+CD8+T cells from dLN of CT26 tumor-bearing mice treated with anti-PD-L1, anti-TIGIT, or anti-PD-L1 + anti-TIGIT with or without FTY720 (FTY) that expressed CD226. p-values are indicated where differences between two groups were determined by two-way unpaired Student’s t-test to be statistically significant. FIG.5B is a set of plots showing the proportion of CD226+(left panel) or CD226- (right panel) gp70+CD8+T cells from dLN of CT26 tumor-bearing mice treated with anti-PD-L1, anti-TIGIT, or anti-PD- L1 + anti-TIGIT with or without FTY720 (FTY) that expressed Ki67. FIG.5C is a set of plots showing the proportion of CD226+(left panel) or CD226- (right panel) gp70+CD8+T cells from dLN of CT26 tumor-bearing mice treated with anti-PD-L1, anti-TIGIT, or anti-PD- L1 + anti-TIGIT with or without FTY720 (FTY) that had a naïve phenotype. FIG.5D is a set of plots showing the proportion of CD226+(left panel) or CD226- (right panel) gp70+CD8+T cells from dLN of CT26 tumor-bearing mice treated with anti-PD-L1, anti-TIGIT, or anti-PD- L1 + anti-TIGIT with or without FTY720 (FTY) that had a cytotoxic CD8+T effector / memory cell (Teff / Tem) phenotype. FIG.5E is a set of plots showing the proportion of CD226+(left panel) or CD226- (right panel) gp70+CD8+T cells from dLN of CT26 tumor-bearing mice treated with anti-PD-L1, anti-TIGIT, or anti-PD- L1 + anti-TIGIT with or without FTY720 (FTY) that expressed PD-1. FIG.5F is a set of plots showing the proportion of CD226+(left panel) or CD226- (right panel) gp70+CD8+T cells from dLN of CT26 tumor-bearing mice treated with anti-PD-L1, anti-TIGIT, or anti-PD- L1 + anti-TIGIT with or without FTY720 (FTY) that expressed TCF1 and Tim3. FIG.5G is a set of plots showing the proportion of CD226+(left panel) or CD226- (right panel) gp70+CD8+T cells from dLN of CT26 tumor-bearing mice treated with anti-PD-L1, anti-TIGIT, or anti-PD- L1 + anti-TIGIT with or without FTY720 (FTY) that expressed Tox. FIG.5H is a plot showing the proportion of gp70+CD8+T cells from tumor tissue of CT26 tumor- bearing mice treated with anti-PD-L1, anti-TIGIT, or anti-PD-L1 + anti-TIGIT with or without FTY720 (FTY) that expressed CD226. PATENT Attorney Docket No.: 50474-320WO2 Genentech Docket No.: P38318-WO FIG.5I is a set of plots showing the proportion of CD226+(left panel) or CD226- (right panel) gp70+CD8+T cells from tumor tissue of CT26 tumor-bearing mice treated with anti-PD-L1, anti-TIGIT, or anti-PD-L1 + anti-TIGIT with or without FTY720 (FTY) that expressed Ki67. FIG.5J is a set of plots showing the proportion of CD226+(left panel) or CD226- (right panel) gp70+CD8+T cells from tumor tissue of CT26 tumor-bearing mice treated with anti-PD-L1, anti-TIGIT, or anti-PD-L1 + anti-TIGIT with or without FTY720 (FTY) that expressed TCF1 and Tim3. FIG.5K is a set of plots showing the proportion of CD226+(left panel) or CD226- (right panel) gp70+CD8+T cells from tumor tissue of CT26 tumor-bearing mice treated with anti-PD-L1, anti-TIGIT, or anti-PD-L1 + anti-TIGIT with or without FTY720 (FTY) that expressed Tox. FIG.5L is a set of plots showing the proportion of dLN (left panel) or tumor (right panel) gp70+CD8+T cells from CT26 tumor-bearing mice treated with anti-PD-L1 + anti-TIGIT, anti-PD-L1 + anti- TIGIT + anti-CD226, or a control that expressed TCF1 and Tim3. FIG.5M is a set of plots showing the proportion of dLN (left panel) or tumor (right panel) gp70+CD8+T cells from CT26 tumor-bearing mice treated with anti-PD-L1 + anti-TIGIT, anti-PD-L1 + anti- TIGIT + anti-CD226, or a control that expressed Tox. FIG.6A is a set of box-and-whisker plots showing associations between levels of the indicated human gene signature scores in baseline tumor bulk RNA-seq samples from the Phase 2 CITYSCAPE non-small cell lung cancer (NSCLC) trial and clinical response to tiragolumab plus atezolizumab. Patients, irrespective of treatment arm, were separated on the basis of clinical response (CRPR, complete response / partial response; SDPD, stable disease / progressive disease). p-values are indicated for statistically significant differences by two-tailed t-test. FIG.6B is a set of box-and-whisker plots showing associations between expression levels of the indicated individual human genes in baseline tumor bulk RNA-seq samples from Phase 2 CITYSCAPE NSCLC trial patients that were treated with tiragolumab plus atezolizumab or placebo plus atezolizumab, separated on the basis of clinical response. FIG.6C is a forest plot showing association of high or low expression of indicated individual human gene with overall survival (OS) hazard ratio (HR) in tiragolumab plus atezolizumab (T+A) or placebo plus atezolizumab (P+A) treatment groups. Mean HR with 95% confidence intervals and p- values are shown. FIG.6D is a set of Kaplan-Meier (K-M) curves showing the probability of OS in P+A or T+A treatment groups dichotomized on the basis of high or low expression of indicated gene. p-value is from a log-rank test with the null hypothesis that there is no difference between the groups. FIG.6E is a set of box-and-whisker plots showing a gene score calculated using the average expression of the CD8 gene panel comprised of CCR7, CXCR3, CXCR6 and CCL5 (top) or CXCR3, CXCR6 and CCL5 (bottom) in tumor bulk RNA-seq samples from patients treated with tiragolumab plus atezolizumab separated on the basis of clinical response. FIG.6F is a forest plot showing association of high or low expression of the indicated composite gene scores with OS HR in T+A or P+A treatment groups. Mean HR with 95% confidence intervals and p- values are shown. PATENT Attorney Docket No.: 50474-320WO2 Genentech Docket No.: P38318-WO FIG.6G is a set of K-M curves showing the probability of OS in P+A or T+A treatment groups dichotomized on the basis of high or low composite gene score. p-value is from a log-rank test with the null hypothesis that there is no difference between the groups. FIG.7A is a set of diagrams showing experimental schema for tumor growth and pharmacodynamic (PD) analysis for the CT26 and EO771 studies (left); delayed FTY720 treatment in the CT26 model (middle); and multi-omic analysis of T cells in the CT26 tumor model (right). FIG.7B is a set of graphs showing tumor volume (mm3) (log2 scale) over time in C57BL / 6 mice that were inoculated in mammary fat pad with EO771 tumor cells, treated with an isotype control anti-PD- L1, anti-TIGIT, or the combination of anti-PD-L1 and anti-TIGIT antibodies, with or without FTY720. Grouped analysis (left panel) and growth curves for each individual animal (n = 10 per group) (right panel) are shown. Data shown are representative of two independent experiments. FIG.7C is a set of plots showing the total numbers of CD8+T cells, CD4+T cells, or Tregs in dLN (top panels) or tumor (bottom panels) of CT26 tumor-bearing mice treated with isotype control, anti-PD- L1, anti-TIGIT, or the combination, with or without FTY720. n = 5 mice per group, mean ± s.d. are represented by bars and whiskers. Data are representative of three independent experiments. FIG.7D is a set of bar graphs showing the frequency of CD8+T cells that had positive staining for the gp70-specific tetramer in dLN (left panel); the number of CD8+T cells with positive staining for the gp70-specific tetramer in blood (right panel); and the frequency of CD8+T cells with positive staining for the gp70-specific tetramer in tumor (right panel) in BALB / c CT26 tumor model mice treated with isotype control, anti-PD-L1 (denoted as aPDL1 or aP), anti-TIGIT (denoted as aTIGIT or aT), or the combination of anti-PD-L1 and anti-TIGIT antibodies, with or without FTY720. Data are a compilation of 2 (blood) or 3 (dLN, tumor) independent experiments (n = 5 per group per experiment), with each dot representing one animal. Bars represent mean, whiskers represent s.d. p-values are indicated where differences between two selected groups were determined by Mann-Whitney test to be statistically significant. *, p < 0.05; **, p < 0.01; ***, p < 0.001; ****, p < 0.0001. Fig.7E is a bar graph showing quantitation of CD8+T cells producing IFN-g and TNF-a as a percentage of total CD8+tumor-infiltrating lymphocytes (TILs) in BALB / c CT26 tumor model mice treated with an isotype control, anti-PD-L1, anti-TIGIT, and / or FTY720. Data are a compilation of 2 independent experiments (n = 5 per group per experiment). p-values are indicated where differences between two selected groups were determined by Mann-Whitney test to be statistically significant. *, p < 0.05; **, p < 0.01; ***, p < 0.001; ****, p < 0.0001. FIG.8A is a set of representative dot plots showing IFN-g and TNF-a intracellular staining in CD8+T cells from tumor. FIG.8B is a set of representative dot plots for CD226 and PD-1 co-expression on CD8+T cells in dLN (top) and for Tim3 and PD-1 co-expression on CD8+T cells in dLN (bottom). FIG.8C is a set of representative dot plots for CD226 and LAG3 co-expression on CD8+T cells in tumor (top) and for Tim3 and PD-1 co-expression on CD8+T cells in tumor (bottom). FIG.8D is a set of representative dot plots for TCF1 and Tox co-expression on CD8+T cells in dLN (top) or in tumor (bottom). PATENT Attorney Docket No.: 50474-320WO2 Genentech Docket No.: P38318-WO FIG.8E is a set of representative dot plots for SLAMF6 and TCF1 co-expression on CD8+T cells in tumor. FIG.8F is a set of representative dot plots for CD226 and gp70 tetramer co-expression on CD8+T cells in dLN (top) or tumor (middle), or gp70 tetramer staining on CD8+T cells in blood (bottom). FIG.9A is a set of images showing T cell clusters representing CD8+T cells, CD4+T cells, and regulatory T cells in 305,908 total T cells pooled from CT26 tumor, dLN, and blood from 31 mice. 10 CD8+T cell clusters (Ccl5-1, Ribo-2, Ccl5-3, CD8-4, CD8-5, Mitotic-9, Mitotic-12, Xcl1-13, Ifn-15, and Ly6a-16), four conventional CD4+T cell clusters (CD40Ig-0, CD40Ig-7, Vim-11, and Stat1-14), two regulatory T (Treg) cell clusters (Treg-6, Treg-8), three clusters of mitotic cells (Mitotic-9, Mitotic-12, and Mitotic-20), two clusters of dying cells (Dying-10 and Dying-17), and several clusters with no clear phenotype (Gxp1-19, CD74-18, and CD74-21) were classified. CD8a expression, granzyme B expression, tissue source, treatment group (Group), clone size, ADT counts, and gp70 antigen specificity projections on UMAP are shown as indicated. FIG.9B is a set of images showing CITE-seq relative expression levels for the indicated markers projected on a UMAP. FIG.10A is a set of images showing relative expression levels of the indicated markers, as measured by CITE-seq, projected on UMAPs comprised of CD8+T cells from CT26 tumor, dLN, and blood. FIG.10B is a heatmap showing relative CITE-seq marker expression levels in the indicated tissues under various treatment conditions. FIG.11A is a set of heatmaps showing cross-labelling of CD8+T cell clusters (rows) to reference gene signatures (columns), taken from the analyses of Huang et al., Cell, 185: 1-18, 2022; Deak et al., Nature, 610: 173–181, 2022); Hashimoto et al., Nature, 610: 173–181, 2022; and Daniel et al., Nat Immunol, 23: 1614-1627, 2022, with intensities indicating normalized frequency. FIG.11B is a set of UMAPs showing cluster composition in dLN (lymph), tumor, and blood from CT26 tumor-bearing mice treated with isotype control, anti-PD-L1, anti-TIGIT, combination, or combination with FTY720. FIG.12A is a set of scatterplots showing primary clusters of each of the indicated individual clonotypes in dLN and blood at day 7. The shade of the circles denotes cluster designation as shown in Fig.3D. FIG.12B is a set of stacked bar graphs showing cluster composition for the 50 largest clonotypes from tumor (upper panels), lymph node (middle panels), or blood at day 7 (lower panels) of CT26 tumor- bearing mice treated with isotype control, anti-PD-L1, anti-TIGIT, combination, or combination with FTY720, shown as absolute numbers. Cluster identity is indicated by shade. FIG.12C is a set of stacked bar graphs showing cluster composition for the 50 largest clonotypes from tumor (upper panels), lymph node (middle panels), or blood at day 7 (lower panels) of CT26 tumor- bearing mice treated with isotype control, anti-PD-L1, anti-TIGIT, combination, or combination with FTY720, normalized against the total number of cells for each individual clonotype (total cell number = 1). Cluster identity is indicated by shade. PATENT Attorney Docket No.: 50474-320WO2 Genentech Docket No.: P38318-WO FIG.13A is a heatmap showing relative co-occurrence relationships within or between dLN, blood, and tumors for CD8+T cells clusters from CT26 tumor-bearing mice. Greater intensity of co- occurrence between two clusters indicates greater similarity, indicative of shared differentiation trajectory. FIG.13B is a heatmap showing clusters defined using metadata from Li et al., J Exp Med, 219: e20210749, 2022, wherein CD8T1 are likely naïve, CD8T2 has Tscm / memory properties, CD8T4 has activated effector cell properties, and CD8T5 has an exhausted phenotype. CD8T1 and CD8T2 were described as T cells that recently entered the tumor, while CD8T4 and CD8T5 were cells resident in tumor. CD8T2 also have the capacity to recirculate from tumor to dLN. FIG.14A is a set of charts showing the frequencies of CD8+T cells in dLN (left) or tumor (right) as a percentage of CD45+cells in mice with established EO771 tumors that were treated with an isotype control Ab or anti-TIGIT combined with anti-PD-L1. dLN and tumors were collected on day 7 post- treatment for phenotypic characterization of CD8+T cells by flow cytometry. n = 4 per group; mean and s.d. are shown as bar and whiskers; data are representative of one of two independent experiments. p- values are indicated where differences were determined by unpaired t-test to be statistically significant. FIG.14B is a set of charts showing the frequencies of CD8+T cells expressing CD226 in dLN (left) or tumor (right) as a percentage of CD45+cells in mice with established EO771 tumors that were treated with an isotype control Ab or anti-TIGIT combined with anti-PD-L1. dLN and tumors were collected on day 7 post-treatment for phenotypic characterization of CD8+T cells by flow cytometry. n = 4 per group; mean and s.d. are shown as bar and whiskers; data are representative of one of two independent experiments. p-values are indicated where differences were determined by unpaired t-test to be statistically significant. FIG.14C is a set of charts showing the frequencies of CD8+T cells positively stained with tetramer against EO771-specific antigen p15E in dLN (left) or tumor (right) as a percentage of CD45+cells in mice with established EO771 tumors that were treated with an isotype control Ab or anti-TIGIT combined with anti-PD-L1. dLN and tumors were collected on day 7 post-treatment for phenotypic characterization of CD8+T cells by flow cytometry. n = 4 per group; mean and s.d. are shown as bar and whiskers; data are representative of one of two independent experiments. p-values are indicated where differences were determined by unpaired t-test to be statistically significant. FIG.14D is a set of charts showing the frequencies of p15E+CD8+T cells expressing CD226 in dLN (left) or tumor (right) as a percentage of CD45+cells in mice with established EO771 tumors that were treated with an isotype control Ab or anti-TIGIT combined with anti-PD-L1. dLN and tumors were collected on day 7 post-treatment for phenotypic characterization of CD8+T cells by flow cytometry. n = 4 per group; mean and s.d. are shown as bar and whiskers; data are representative of one of two independent experiments. p-values are indicated where differences were determined by unpaired t-test to be statistically significant. FIG.14E is a set of charts showing the frequencies of CD226+(left) or CD226- (right) p15E+CD8+Teff / Tem cells co-expressing TCF1 and Tim3 in dLN (left) or tumor (right) as a percentage of CD45+cells in mice with established EO771 tumors that were treated with an isotype control Ab or anti-TIGIT combined with anti-PD-L1. dLN and tumors were collected on day 7 post-treatment for phenotypic characterization of CD8+T cells by flow cytometry. n = 4 per group; mean and s.d. are shown as bar and PATENT Attorney Docket No.: 50474-320WO2 Genentech Docket No.: P38318-WO whiskers; data are representative of one of two independent experiments. p-values are indicated where differences were determined by unpaired t-test to be statistically significant. FIG.14F is a set of charts showing the frequencies of CD226+(left) or CD226- (right) p15E+CD8+Teff / Tem cells co-expressing Tox in dLN (left) or tumor (right) as a percentage of CD45+cells in mice with established EO771 tumors that were treated with an isotype control Ab or anti-TIGIT combined with anti- PD-L1. dLN and tumors were collected on day 7 post-treatment for phenotypic characterization of CD8+T cells by flow cytometry. n = 4 per group; mean and s.d. are shown as bar and whiskers; data are representative of one of two independent experiments. p-values are indicated where differences were determined by unpaired t-test to be statistically significant. FIG.15A is an image showing scRNA-seq of 144,413 human CD8+T cells from blood of patients in a Ph1b NSCLC study of tiragolumab plus atezolizumab (T+A) in which human genes were renamed to their mouse ortholog (if present) and gene expression was normalized before sample integration and projection onto a mouse CD8+T cell reference UMAP. FIG.15B is a set of plots showing predicted cell type scores for mapped human CD8+T cells for each assigned mouse CD8+T cell reference cluster. FIG.15C is a set of box-and-whisker plots showing frequencies of the indicated human predicted clusters in patients with complete response or partial response (CRPR) compared to stable disease or progressive disease (SDPD) on cycle 2 day 1 of treatment with T+A in the Ph1b study. Percent total was calculated as the percentage of the cluster in total CD8+T cells for each patient. FIG.15D is a forest plot showing the association between high or low expression of the top corresponding human 18-20 signature genes (signature gene score) from each mouse CD8+T cell cluster or CD8A and overall survival (OS) hazard ratio (HR) T+A or placebo plus atezolizumab (P+A) treatment groups in the Ph2 CITYSCAPE study. Mean HR with 95% confidence intervals and p-values are shown. FIG.15E is a set of Kaplan-Meier curves showing OS probability in P+A or T+A treatment groups dichotomized on the basis of high or low CD8+T cell cluster gene scores from each reference cluster. p- value is from a log-rank test with the null hypothesis that there is no difference between the groups. FIG.15F is a set of Kaplan-Meier curves comparing progression-free survival (PFS, left) or OS (right) in patients from the phase 3 NSCLC OAK study who received atezolizumab monotherapy. Patients were dichotomized by median gene score calculated using the average expression of the CD8 gene panel comprised of CCR7, CXCR3, CXCR6 and CCL5. FIG.16 is a diagram showing a model of anti-TIGIT plus anti-PD-L1 combination effects on tumor-specific CD8+T cell differentiation in the syngeneic mouse CT26 tumor model. Combination treatment drives dual expansion of tumor-specific gp70+CD8+T cell clones in both dLN and tumor, and egress from dLN and trafficking to tumor is required initially until the tumor is sufficiently seeded by infiltrating cells. Dual expanded gp70+CD8+T cell clones highly express CD226 and Ccl5 and have properties of stem cell-like memory / precursor exhausted (Tscm / Tpex) cells such as TCF-1 expression and reduced exhaustion programming as marked by reduction in Tox expression, thereby increasing the pool of CD8+T cells with antitumor effector activity at the expense of exhaustion. Anti-TIGIT alone phenocopies gp70+CD8+T cells responding to combination treatment but does not drive robust dual PATENT Attorney Docket No.: 50474-320WO2 Genentech Docket No.: P38318-WO expansion. Anti-PD-L1 alone does not promote dual expansion nor does it confer protection from the exhaustion pathway. FIG.17 is a set of Kaplan-Meier curves showing progression-free survival (PFS, left) or OS (right) in the PD-L1-positive subset (TPS ≥ 1%) of patients from the IMpower110 study who received atezolizumab monotherapy. Patients were dichotomized by median gene score calculated using the average expression of the CD8 gene panel comprised of CCR7, CXCR3, CXCR6 and CCL5. DETAILED DESCRIPTION I. GENERAL TECHNIQUES AND DEFINITIONS The techniques and procedures described or referenced herein are generally well understood and commonly employed using conventional methodology by those skilled in the art, such as, for example, the widely utilized methodologies described in Sambrook et al., Molecular Cloning: A Laboratory Manual 3d edition (2001) Cold Spring Harbor Laboratory Press, Cold Spring Harbor, N.Y.; Current Protocols in Molecular Biology (F.M. Ausubel, et al. eds., (2003)); the series Methods in Enzymology (Academic Press, Inc.): PCR 2: A Practical Approach (M.J. MacPherson, B.D. Hames and G.R. Taylor eds. (1995)), Harlow and Lane, eds. (1988) Antibodies, A Laboratory Manual, and Animal Cell Culture (R.I. Freshney, ed. (1987)); Oligonucleotide Synthesis (M.J. Gait, ed., 1984); Methods in Molecular Biology, Humana Press; Cell Biology: A Laboratory Notebook (J.E. Cellis, ed., 1998) Academic Press; Animal Cell Culture (R.I. Freshney), ed., 1987); Introduction to Cell and Tissue Culture (J.P. Mather and P.E. Roberts, 1998) Plenum Press; Cell and Tissue Culture: Laboratory Procedures (A. Doyle, J.B. Griffiths, and D.G. Newell, eds., 1993-8) J. Wiley and Sons; Handbook of Experimental Immunology (D.M. Weir and C.C. Blackwell, eds.); Gene Transfer Vectors for Mammalian Cells (J.M. Miller and M.P. Calos, eds., 1987); PCR: The Polymerase Chain Reaction, (Mullis et al., eds., 1994); Current Protocols in Immunology (J.E. Coligan et al., eds., 1991); Short Protocols in Molecular Biology (Wiley and Sons, 1999); Immunobiology (C.A. Janeway and P. Travers, 1997); Antibodies (P. Finch, 1997); Antibodies: A Practical Approach (D. Catty., ed., IRL Press, 1988-1989); Monoclonal Antibodies: A Practical Approach (P. Shepherd and C. Dean, eds., Oxford University Press, 2000); Using Antibodies: A Laboratory Manual (E. Harlow and D. Lane (Cold Spring Harbor Laboratory Press, 1999); The Antibodies (M. Zanetti and J. D. Capra, eds., Harwood Academic Publishers, 1995); and Cancer: Principles and Practice of Oncology (V.T. DeVita et al., eds., J.B. Lippincott Company, 1993). It is to be understood that aspects and embodiments of the invention described herein include “comprising,” “consisting,” and “consisting essentially of” aspects and embodiments. As used herein, the singular form “a,” “an,” and “the” includes plural references unless indicated otherwise. The term “about” as used herein refers to the usual error range for the respective value readily known to the skilled person in this technical field. Reference to “about” a value or parameter herein includes (and describes) embodiments that are directed to that value or parameter per se. For example, description referring to “about X” includes description of “X.” The “amount,” “level,” or “expression level,” used herein interchangeably, of a biomarker is a detectable level in a biological sample. “Expression” generally refers to the process by which information (e.g., gene-encoded and / or epigenetic) is converted into the structures present and operating in the cell. PATENT Attorney Docket No.: 50474-320WO2 Genentech Docket No.: P38318-WO Therefore, as used herein, “expression” may refer to transcription into a polynucleotide, translation into a polypeptide, or even polynucleotide and / or polypeptide modifications (e.g., posttranslational modification of a polypeptide). Fragments of the transcribed polynucleotide, the translated polypeptide, or polynucleotide and / or polypeptide modifications (e.g., posttranslational modification of a polypeptide) shall also be regarded as expressed whether they originate from a transcript generated by alternative splicing or a degraded transcript, or from a post-translational processing of the polypeptide, e.g., by proteolysis. “Expressed genes” include those that are transcribed into a polynucleotide as mRNA and then translated into a polypeptide, and also those that are transcribed into RNA but not translated into a polypeptide (for example, transfer and ribosomal RNAs). Expression levels can be measured by methods known to one skilled in the art and also disclosed herein. The terms “detecting” and “detection” are used herein in the broadest sense to include both qualitative and quantitative measurements of a target molecule. Detecting includes identifying the mere presence of the target molecule in a sample as well as determining whether the target molecule is present in the sample at detectable levels. Detecting may be direct or indirect. The presence and / or expression level / amount of various biomarkers described herein in a sample can be analyzed by a number of methodologies, many of which are known in the art and understood by the skilled artisan, including, but not limited to, immunohistochemistry (“IHC”), Western blot analysis, immunoprecipitation, molecular binding assays, ELISA, ELIFA, fluorescence activated cell sorting (“FACS”), MassARRAY, proteomics, quantitative blood based assays (e.g., Serum ELISA), biochemical enzymatic activity assays, in situ hybridization, fluorescence in situ hybridization (FISH), Southern analysis, Northern analysis, whole genome sequencing, massively parallel DNA sequencing (e.g., next-generation sequencing), NANOSTRING®, polymerase chain reaction (PCR) including quantitative real time PCR (qRT-PCR) and other amplification type detection methods, such as, for example, branched DNA, SISBA, TMA and the like, RNA-seq, microarray analysis, gene expression profiling, and / or serial analysis of gene expression (“SAGE”), as well as any one of the wide variety of assays that can be performed by protein, gene, and / or tissue array analysis. Typical protocols for evaluating the status of genes and gene products are found, for example in Ausubel et al., eds., 1995, Current Protocols In Molecular Biology, Units 2 (Northern Blotting), 4 (Southern Blotting), 15 (Immunoblotting) and 18 (PCR Analysis). Multiplexed immunoassays such as those available from Rules Based Medicine or Meso Scale Discovery (“MSD”) may also be used. The term “C-C motif chemokine 5” or “CCL5,” as used herein, broadly refers to any native CCL5 from any mammalian source, including primates (e.g., humans) and rodents (e.g., mice and rats), unless otherwise indicated. The term encompasses full-length CCL5 and isolated regions or domains of CCL5, e.g., the CCL5 ECD. The term also encompasses naturally occurring variants of CCL5, e.g., splice variants or allelic variants. The amino acid sequence of an exemplary human CCL5 is shown under UniProt Accession No. P13501. Minor sequence variations, especially conservative amino acid substitutions of CCL5 that do not affect CCL5 function and / or activity, are also contemplated by the invention. The term “C-X-C chemokine receptor type 3” or “CXCR3,” as used herein, broadly refers to any native CXCR3 from any mammalian source, including primates (e.g., humans) and rodents (e.g., mice PATENT Attorney Docket No.: 50474-320WO2 Genentech Docket No.: P38318-WO and rats), unless otherwise indicated. The term encompasses full-length CXCR3 and isolated regions or domains of CXCR3, e.g., the CXCR3 ECD. The term also encompasses naturally occurring variants of CXCR3, e.g., splice variants or allelic variants. The amino acid sequence of an exemplary human CXCR3 is shown under UniProt Accession No. P49682. Minor sequence variations, especially conservative amino acid substitutions of CXCR3 that do not affect CXCR3 function and / or activity, are also contemplated by the invention. The term “C-X-C chemokine receptor type 6” or “CXCR6,” as used herein, broadly refers to any native CXCR6 from any mammalian source, including primates (e.g., humans) and rodents (e.g., mice and rats), unless otherwise indicated. The term encompasses full-length CXCR6 and isolated regions or domains of CXCR6, e.g., the CXCR6 ECD. The term also encompasses naturally occurring variants of CXCR6, e.g., splice variants or allelic variants. The amino acid sequence of an exemplary human CXCR6 is shown under UniProt Accession No. O00574. Minor sequence variations, especially conservative amino acid substitutions of CXCR6 that do not affect CXCR6 function and / or activity, are also contemplated by the invention. The term “C-C chemokine receptor type 7” or “CCR7,” as used herein, broadly refers to any native CCR7 from any mammalian source, including primates (e.g., humans) and rodents (e.g., mice and rats), unless otherwise indicated. The term encompasses full-length CCR7 and isolated regions or domains of CCR7, e.g., the CCR7 ECD. The term also encompasses naturally occurring variants of CCR7, e.g., splice variants or allelic variants. The amino acid sequence of an exemplary human CCR7 is shown under UniProt Accession No. P32248. Minor sequence variations, especially conservative amino acid substitutions of CCR7 that do not affect CCR7 function and / or activity, are also contemplated by the invention. The term “TIGIT” or “T-cell immunoreceptor with Ig and ITIM domains” as used herein refers to any native TIGIT from any vertebrate source, including mammals such as primates (e.g., humans) and rodents (e.g., mice and rats), unless otherwise indicated. TIGIT is also known in the art as DKFZp667A205, FLJ39873, V-set and immunoglobulin domain-containing protein 9, V-set and transmembrane domain-containing protein 3, VSIG9, VSTM3, and WUCAM. The term encompasses “full-length,” unprocessed TIGIT (e.g., full-length human TIGIT having the amino acid sequence of SEQ ID NO: 1), as well as any form of TIGIT that results from processing in the cell (e.g., processed human TIGIT without a signal sequence, having the amino acid sequence of SEQ ID NO: 2). The term also encompasses naturally occurring variants of TIGIT, e.g., splice variants or allelic variants. The amino acid sequence of an exemplary human TIGIT may be found under UniProt Accession Number Q495A1. The term “PD-L1” or “Programmed Cell Death Ligand 1” refers herein to any native PD-L1 from any vertebrate source, including mammals such as primates (e.g., humans) and rodents (e.g., mice and rats), unless otherwise indicated. PD-L1 is also known in the art as CD274 molecule, CD274 antigen, B7 homolog 1, PDCD1 Ligand 1, PDCD1LG1, PDCD1L1, B7H1, PDL1, programmed death ligand 1, B7-H1, and B7-H. The term also encompasses naturally occurring variants of PD-L1, e.g., splice variants, or allelic variants. The amino acid sequence of an exemplary human PD-L1 may be found under UniProt Accession Number Q9NZQ7 (SEQ ID NO: 3). As used herein, the term “atezolizumab” refers to anti-PD-L1 antagonist antibody having the PATENT Attorney Docket No.: 50474-320WO2 Genentech Docket No.: P38318-WO International Nonproprietary Names for Pharmaceutical Substances (INN) List 112 (WHO Drug Information, Vol.28, No.4, 2014, p.488), or the CAS Registry Number 1380723-44-3. As used herein, “tiragolumab” is a fully human IgG1 / kappa MAb that binds TIGIT and comprises the heavy chain sequence of SEQ ID NO: 4 and the light chain sequence of SEQ ID NO: 5. Tiragolumab comprises two N-linked glycosylation sites (N306) in the Fc domain. Tiragolumab is also described in WHO Drug Information (International Nonproprietary Names for Pharmaceutical Substances), Proposed INN: List 117, Vol.31, No.2, published June 9, 2017 (see page 343). Tiragolumab (Genentech) is also known as MTIG7192A, RG6058, or RO7092284. Tiragolumab is described in PCT Pub. Nos. WO2003072305A8, WO2004024068A3, WO2004024072A3, WO2009126688A2, WO2015009856A2, WO2016011264A1, WO2016109546A2, WO2017053748A2, and WO2019165434A1; US Pub. Nos. 2017 / 0044256, 2017 / 0037127, 2017 / 0145093, 2017 / 260594, 2017 / 0088613, 2018 / 0186875, 2019 / 0119376; and US Pat. Nos. US9873740B2, US10626174B2, US10611836B2, US9499596B2, US8431350B2, US10047158B2, and US10017572B2. As used herein, “administering” is meant a method of giving a dosage of a compound (e.g., tiragolumab and / or atezolizumab) or a composition (e.g., a pharmaceutical composition, e.g., a pharmaceutical composition including an tiragolumab and / or atezolizumab) to a subject. The compounds and / or compositions utilized in the methods described herein can be administered, for example, intravenously (e.g., by intravenous infusion), subcutaneously, intramuscularly, intradermally, percutaneously, intraarterially, intraperitoneally, intralesionally, intracranially, intraarticularly, intraprostatically, intrapleurally, intratracheally, intranasally, intravitreally, intravaginally, intrarectally, topically, intratumorally, peritoneally, subconjunctivally, intravesicularlly, mucosally, intrapericardially, intraumbilically, intraocularly, orally, topically, locally, by inhalation, by injection, by infusion, by continuous infusion, by localized perfusion bathing target cells directly, by catheter, by lavage, in cremes, or in lipid compositions. The method of administration can vary depending on various factors (e.g., the compound or composition being administered and the severity of the condition, disease, or disorder being treated). As used herein, “systemic treatment” refers to a treatment that travels through the bloodstream and is capable of contacting multiple organ systems upon a single administration. The term “systemic treatment” is well understood by those skilled in the art and is equivalent to systemic therapy. A “fixed” or “flat” dose of a therapeutic agent (e.g., tiragolumab or atezolizumab) herein refers to a dose that is administered to a patient without regard for the weight or body surface area (BSA) of the patient. The fixed or flat dose is therefore not provided as a mg / kg dose or a mg / m2dose, but rather as an absolute amount of the therapeutic agent (e.g., mg). As used herein, the term “treatment” or “treating” refers to clinical intervention designed to alter the natural course of the individual or cell being treated during the course of clinical pathology. Desirable effects of treatment include delaying or decreasing the rate of disease progression, ameliorating or palliating the disease state, and remission or improved prognosis. For example, an individual is successfully “treated” if one or more symptoms associated with cancer are mitigated or eliminated, including, but are not limited to, reducing the proliferation of (or destroying) cancerous cells, decreasing symptoms resulting from the disease, increasing the quality of life of those suffering from the disease, PATENT Attorney Docket No.: 50474-320WO2 Genentech Docket No.: P38318-WO decreasing the dose of other medications required to treat the disease, delaying the progression of the disease, and / or prolonging survival of individuals. As used herein, “in conjunction with” refers to administration of one treatment modality in addition to another treatment modality. As such, “in conjunction with” refers to administration of one treatment modality before, during, or after administration of the other treatment modality to the individual. A “disorder” or “disease” is any condition that would benefit from treatment including, but not limited to, disorders that are associated with some degree of abnormal cell proliferation, e.g., cancer, e.g., lung cancer, e.g., non-small cell lung cancer (NSCLC). The terms “cancer” and “cancerous” refer to or describe the physiological condition in mammals that is typically characterized by unregulated cell growth. Examples of cancer include, but are not limited to, carcinoma, lymphoma, blastoma, sarcoma, and leukemia or lymphoid malignancies. More particular examples of such cancers include, but are not limited to lung cancer, such as non-small cell lung cancer (NSCLC), which includes squamous NSCLC or non-squamous NSCLC, including locally advanced unresectable NSCLC (e.g., Stage IIIB NSCLC), or recurrent or metastatic NSCLC (e.g., Stage IV NSCLC). The term “tumor” refers to all neoplastic cell growth and proliferation, whether malignant or benign, and all pre-cancerous and cancerous cells and tissues. The terms “cancer,” “cancerous,” “cell proliferative disorder,” “proliferative disorder,” and “tumor” are not mutually exclusive as referred to herein. As used herein, “metastasis” is meant the spread of cancer from its primary site to other places in the body. Cancer cells can break away from a primary tumor, penetrate into lymphatic and blood vessels, circulate through the bloodstream, and grow in a distant focus (metastasize) in normal tissues elsewhere in the body. Metastasis can be local or distant. Metastasis is a sequential process, contingent on tumor cells breaking off from the primary tumor, traveling through the bloodstream, and stopping at a distant site. At the new site, the cells establish a blood supply and can grow to form a life-threatening mass. Both stimulatory and inhibitory molecular pathways within the tumor cell regulate this behavior, and interactions between the tumor cell and host cells in the distant site are also significant. An “effective amount” of a compound, for example, tiragolumab or atezolizumab, or a composition (e.g., pharmaceutical composition) thereof, is at least the minimum amount required to achieve the desired therapeutic result, such as a measurable increase in overall survival or progression- free survival of a particular disease or disorder (e.g., cancer, e.g., lung cancer (e.g., NSCLC)). An effective amount herein may vary according to factors such as the disease state, age, sex, and weight of the patient, and the ability of the antibody to elicit a desired response in the subject. An effective amount is also one in which any toxic or detrimental effects of the treatment are outweighed by the therapeutically beneficial effects. For prophylactic use, beneficial or desired results include results such as eliminating or reducing the risk, lessening the severity, or delaying the onset of the disease, including biochemical, histological and / or behavioral symptoms of the disease, its complications, and intermediate pathological phenotypes presenting during development of the disease. For therapeutic use, beneficial or desired results include clinical results such as decreasing one or more symptoms resulting from the disease (e.g., reduction or delay in cancer-related pain, symptomatic skeletal-related events (SSE), reduction in symptoms per the European Organization for Research and Treatment of Cancer Quality-of-Life PATENT Attorney Docket No.: 50474-320WO2 Genentech Docket No.: P38318-WO Questionnaire (EORTC QLQ-C30, e.g., fatigue, nausea, vomiting, pain, dyspnea, insomnia, appetite loss, constipation, diarrhea, or general level of physical emotional, cognitive, or social functioning), reduction in pain as measured by, e.g., the 10-point pain severity (measured at its worst) numerical rating scale (NRS), and / or reduction in symptoms associated with lung cancer per the health-related quality of life (HRQoL) questionnaire as assessed by symptoms in lung cancer (SILC) scale (e.g., time to deterioration (TTD) in cough dyspenea and chest pain), increasing the quality of life of those suffering from the disease, decreasing the dose of other medications required to treat the disease, enhancing effect of another medication such as via targeting, delaying the progression of the disease (e.g. progression-free survival or radiographic progression-free survival (rPFS); delay of unequivocal clinical progression (e.g., cancer-related pain progression, symptomatic skeletal-related event, deterioration in Eastern Cooperative Group Oncology Group (ECOG) Performance Status (PS) (e.g., how the disease affects the daily living abilities of the patient), and / or initiation of next systemic anti-cancer therapy), and / or delaying time to lung-specific antigen progression), and / or prolonging survival. In the case of cancer or tumor, an effective amount of the drug may have the effect in reducing the number of cancer cells; reducing the tumor size; inhibiting (i.e., slow to some extent or desirably stop) cancer cell infiltration into peripheral organs; inhibit (i.e., slow to some extent and desirably stop) tumor metastasis; inhibiting to some extent tumor growth; and / or relieving to some extent one or more of the symptoms associated with the disorder. An effective amount can be administered in one or more administrations. For purposes of this invention, an effective amount of drug, compound, or pharmaceutical composition is an amount sufficient to accomplish prophylactic or therapeutic treatment either directly or indirectly. As is understood in the clinical context, an effective amount of a drug, compound, or pharmaceutical composition may or may not be achieved in conjunction with another drug, compound, or pharmaceutical composition. Thus, an “effective amount” may be considered in the context of administering one or more therapeutic agents, and a single agent may be considered to be given in an effective amount if, in conjunction with one or more other agents, a desirable result may be or is achieved. “Individual response” or “response” can be assessed using any endpoint indicating a benefit to the subject, including, without limitation, (1) inhibition, to some extent, of disease progression (e.g., progression of cancer, e.g., lung cancer (e.g., NSCLC)), including slowing down and complete arrest; (2) a reduction in tumor size; (3) inhibition (i.e., reduction, slowing down or complete stopping) of cancer cell infiltration into adjacent peripheral organs and / or tissues; (4) inhibition (i.e., reduction, slowing down or complete stopping) of metastasis; (5) relief, to some extent, of one or more symptoms associated with the disease or disorder (e.g., cancer, e.g., lung cancer (e.g., NSCLC)); (6) increase or extension in the length of survival, including overall survival and progression-free survival; and / or (9) decreased mortality at a given point of time following treatment. As used herein, “complete response” or “CR” refers to disappearance of all target lesions. As used herein, “partial response” or “PR” refers to at least a 30% decrease in the sum of the longest diameters (SLD) of target lesions, taking as reference the baseline SLD. As used herein, “objective response rate” (ORR) refers to the sum of complete response (CR) rate and partial response (PR) rate. PATENT Attorney Docket No.: 50474-320WO2 Genentech Docket No.: P38318-WO An “effective response” of a subject or a subject’s “responsiveness” to treatment with a medicament and similar wording refers to the clinical or therapeutic benefit imparted to a subject as risk for, or suffering from, a disease or disorder, such as cancer. In one embodiment, such benefit includes any one or more of: extending survival (including overall survival and progression free survival); resulting in an objective response (including a complete response or a partial response); or improving signs or symptoms of cancer. A subject who “does not have an effective response” to treatment refers to a subject who does not have any one of extending survival (including overall survival and progression free survival); resulting in an objective response (including a complete response or a partial response); or improving signs or symptoms of cancer. As used herein, “survival” refers to the patient remaining alive, and includes overall survival as well as progression-free survival. As used herein, “overall survival” (OS) refers to the percentage of subjects in a group who are alive after a particular duration of time, e.g., 1 year or 5 years from the time of diagnosis or treatment. As used herein, “progression-free survival” (PFS) refers to the length of time during and after treatment during which the disease being treated (e.g., cancer, e.g., lung cancer (e.g., NSCLC)) does not get worse. Progression-free survival may include the amount of time patients have experienced a complete response or a partial response, as well as the amount of time patients have experienced stable disease. As used herein, “stable disease” or “SD” refers to neither sufficient shrinkage of target lesions to qualify for PR, nor sufficient increase to qualify for PD, taking as reference the smallest SLD since the treatment started. As used herein, “progressive disease” or “PD” refers to at least a 20% increase in the SLD of target lesions, taking as reference the smallest SLD recorded since the treatment started or the presence of one or more new lesions. As used herein, “delaying progression” of a disorder or disease means to defer, hinder, slow, retard, stabilize, and / or postpone development of the disease or disorder (e.g., cancer, e.g., lung cancer (e.g., NSCLC)). This delay can be of varying lengths of time, depending on the history of the disease and / or subject being treated. As is evident to one skilled in the art, a sufficient or significant delay can, in effect, encompass prevention, in that the subject does not develop the disease. For example, in a late stage cancer, development of central nervous system (CNS) metastasis, may be delayed. By “extending survival” is meant increasing overall or progression free survival in a treated patient relative to an untreated patient (e.g., relative to a patient not treated with the medicament), or relative to a patient who does not express a biomarker at the designated level, and / or relative to a patient treated with an approved anti-tumor agent. An objective response refers to a measurable response, including complete response (CR) or partial response (PR). As used herein, “hazard ratio” or “HR” is a statistical definition for rates of events. For the purpose of the invention, hazard ratio is defined as representing the probability of an event (e.g., PFS or OS) in the experimental (e.g., treatment) group / arm divided by the probability of an event in the control group / arm at any specific point in time. An HR with a value of 1 indicates that the relative risk of an PATENT Attorney Docket No.: 50474-320WO2 Genentech Docket No.: P38318-WO endpoint (e.g., death) is equal in both the “treatment” and “control” groups; a value greater than 1 indicates that the risk is greater in the treatment group relative to the control group; and a value less than 1 indicates that the risk is greater in the control group relative to the treatment group. “Hazard ratio” in progression-free survival analysis (i.e., PFS HR) is a summary of the difference between two progression- free survival curves, representing the reduction in the risk of death on treatment compared to control, over a period of follow-up. “Hazard ratio” in overall survival analysis (i.e., OS HR) is a summary of the difference between two overall survival curves, representing the reduction in the risk of death on treatment compared to control, over a period of follow-up. As used herein, the “Ventana SP263 IHC assay” (also referred to herein as the Ventana SP263 CDx assay) is conducted according to the Ventana PD-L1 (SP263) Assay package insert (Tucson, AZ: Ventana Medical Systems, Inc.), which is incorporated herein by reference in its entirety. As used herein, the “Ventana SP142 IHC assay” is conducted according to the Ventana PD-L1 (SP142) Assay package insert (Tucson, AZ: Ventana Medical Systems, Inc.), which is incorporated herein by reference in its entirety. As used herein, the “pharmDx 22C3 IHC assay” is conducted according to the PD-L1 IHC 22C3 pharmDx package insert (Carpinteria, CA: Dako, Agilent Pathology Solutions), which is incorporated herein by reference in its entirety. A “tumor-infiltrating immune cell,” as used herein, refers to any immune cell present in a tumor or a sample thereof. Tumor-infiltrating immune cells include, but are not limited to, intratumoral immune cells, peritumoral immune cells, other tumor stroma cells (e.g., fibroblasts), or any combination thereof. Such tumor-infiltrating immune cells can be, for example, T lymphocytes (such as CD8+ T lymphocytes and / or CD4+ T lymphocytes), B lymphocytes, or other bone marrow-lineage cells, including granulocytes (e.g., neutrophils, eosinophils, and basophils), monocytes, macrophages, dendritic cells (e.g., interdigitating dendritic cells), histiocytes, and natural killer cells. The term “biomarker,” as used herein, refers to an indicator, e.g., predictive, diagnostic, and / or prognostic, which can be detected in a sample. In some embodiments, a biomarker is a gene. Biomarkers include, but are not limited to, polypeptides, polynucleotides (e.g., DNA, and / or RNA), polynucleotide copy number alterations (e.g., DNA copy numbers), polypeptide and polynucleotide modifications (e.g., posttranslational modifications), carbohydrates, and / or glycolipid-based molecular markers. As used herein, “subject” or “individual” means a mammal, including, but not limited to, a human or non-human mammal, such as a bovine, equine, canine, ovine, or feline. In some embodiments, the subject is a human. Patients are also subjects herein. The term “sample,” as used herein, refers to a composition that is obtained or derived from a subject and / or individual of interest that contains a cellular and / or other molecular entity that is to be characterized and / or identified, for example based on physical, biochemical, chemical and / or physiological characteristics. For example, the phrase “tumor sample,” “disease sample,” and variations thereof refers to any sample obtained from a subject of interest that would be expected or is known to contain the cellular and / or molecular entity that is to be characterized. In some embodiments, the sample is a tumor tissue sample (e.g., a lung cancer sample (e.g., a NSCLC sample)). Other samples include, PATENT Attorney Docket No.: 50474-320WO2 Genentech Docket No.: P38318-WO but are not limited to, primary or cultured cells or cell lines, cell supernatants, cell lysates, platelets, serum, plasma, vitreous fluid, lymph fluid, synovial fluid, follicular fluid, seminal fluid, amniotic fluid, milk, whole blood, blood-derived cells, urine, cerebro-spinal fluid, saliva, sputum, tears, perspiration, mucus, stool, tumor lysates, and tissue culture medium, tissue extracts such as homogenized tissue, cellular extracts, and combinations thereof. In some aspects, the sample is a tumor draining lymph node (dLN) sample. The terms “tissue sample” and “cell sample” mean a collection of similar cells obtained from a tissue of a subject or individual. The source of the tissue or cell sample may be solid tissue as from a fresh, frozen, and / or preserved organ, tissue sample, biopsy, and / or aspirate; blood or any blood constituents such as plasma; bodily fluids such as cerebral spinal fluid, amniotic fluid, peritoneal fluid, or interstitial fluid; cells from any time in gestation or development of the subject. The tissue sample may also be primary or cultured cells or cell lines. Optionally, the tissue or cell sample is obtained from a diseased tissue / organ. The tissue sample may contain compounds which are not naturally intermixed with the tissue in nature such as preservatives, anticoagulants, buffers, fixatives, nutrients, antibiotics, or the like. A “reference sample,” “reference cell,” “reference tissue,” “control sample,” “control cell,” or “control tissue,” as used herein, refers to a sample, cell, tissue, standard, or level that is used for comparison purposes. In one embodiment, a reference sample, reference cell, reference tissue, control sample, control cell, or control tissue is obtained from a healthy and / or non-diseased part of the body (e.g., tissue or cells) of the same subject. For example, healthy and / or non-diseased cells or tissue adjacent to the diseased cells or tissue (e.g., cells or tissue adjacent to a tumor). In another embodiment, a reference sample is obtained from an untreated tissue and / or cell of the body of the same subject. In yet another embodiment, a reference sample, reference cell, reference tissue, control sample, control cell, or control tissue is obtained from a healthy and / or non-diseased part of the body (e.g., tissues or cells) of a subject who is not the subject. In even another embodiment, a reference sample, reference cell, reference tissue, control sample, control cell, or control tissue is obtained from an untreated tissue and / or cell of the body of an individual who is not the subject. The term “protein,” as used herein, refers to any native protein from any vertebrate source, including mammals such as primates (e.g., humans) and rodents (e.g., mice and rats), unless otherwise indicated. The term encompasses “full-length,” unprocessed protein as well as any form of the protein that results from processing in the cell. The term also encompasses naturally occurring variants of the protein, e.g., splice variants or allelic variants. “Polynucleotide” or “nucleic acid,” as used interchangeably herein, refers to polymers of nucleotides of any length, and include DNA and RNA. The nucleotides can be deoxyribonucleotides, ribonucleotides, modified nucleotides or bases, and / or their analogs, or any substrate that can be incorporated into a polymer by DNA or RNA polymerase, or by a synthetic reaction. Thus, for instance, polynucleotides as defined herein include, without limitation, single- and double-stranded DNA, DNA including single- and double-stranded regions, single- and double-stranded RNA, and RNA including single- and double-stranded regions, hybrid molecules comprising DNA and RNA that may be single- stranded or, more typically, double-stranded or include single- and double-stranded regions. In addition, PATENT Attorney Docket No.: 50474-320WO2 Genentech Docket No.: P38318-WO the term “polynucleotide” as used herein refers to triple-stranded regions comprising RNA or DNA or both RNA and DNA. The strands in such regions may be from the same molecule or from different molecules. The regions may include all of one or more of the molecules, but more typically involve only a region of some of the molecules. One of the molecules of a triple-helical region often is an oligonucleotide. The terms “polynucleotide” and “nucleic acid” specifically includes mRNA and cDNAs. A polynucleotide may comprise modified nucleotides, such as methylated nucleotides and their analogs. If present, modification to the nucleotide structure may be imparted before or after assembly of the polymer. The sequence of nucleotides may be interrupted by non-nucleotide components. A polynucleotide may be further modified after synthesis, such as by conjugation with a label. Other types of modifications include, for example, “caps,” substitution of one or more of the naturally-occurring nucleotides with an analog, internucleotide modifications such as, for example, those with uncharged linkages (e.g., methyl phosphonates, phosphotriesters, phosphoamidates, carbamates, and the like) and with charged linkages (e.g., phosphorothioates, phosphorodithioates, and the like), those containing pendant moieties, such as, for example, proteins (e.g., nucleases, toxins, antibodies, signal peptides, poly-L-lysine, and the like), those with intercalators (e.g., acridine, psoralen, and the like), those containing chelators (e.g., metals, radioactive metals, boron, oxidative metals, and the like), those containing alkylators, those with modified linkages (e.g., alpha anomeric nucleic acids), as well as unmodified forms of the polynucleotide(s). Further, any of the hydroxyl groups ordinarily present in the sugars may be replaced, for example, by phosphonate groups, phosphate groups, protected by standard protecting groups, or activated to prepare additional linkages to additional nucleotides, or may be conjugated to solid or semi-solid supports. The 5’ and 3’ terminal OH can be phosphorylated or substituted with amines or organic capping group moieties of from 1 to 20 carbon atoms. Other hydroxyls may also be derivatized to standard protecting groups. Polynucleotides can also contain analogous forms of ribose or deoxyribose sugars that are generally known in the art, including, for example, 2’-O- methyl-, 2’-O-allyl-, 2’-fluoro-, or 2’-azido-ribose, carbocyclic sugar analogs, α-anomeric sugars, epimeric sugars such as arabinose, xyloses or lyxoses, pyranose sugars, furanose sugars, sedoheptuloses, acyclic analogs, and abasic nucleoside analogs such as methyl riboside. One or more phosphodiester linkages may be replaced by alternative linking groups. These alternative linking groups include, but are not limited to, embodiments wherein phosphate is replaced by P(O)S (“thioate”), P(S)S (“dithioate”), “(O)NR2 (“amidate”), P(O)R, P(O)OR’, CO or CH2 (“formacetal”), in which each R or R’ is independently H or substituted or unsubstituted alkyl (1-20 C) optionally containing an ether (-O-) linkage, aryl, alkenyl, cycloalkyl, cycloalkenyl or araldyl. Not all linkages in a polynucleotide need be identical. The preceding description applies to all polynucleotides referred to herein, including RNA and DNA. “Carriers” as used herein include pharmaceutically acceptable carriers, excipients, or stabilizers that are nontoxic to the cell or mammal being exposed thereto at the dosages and concentrations employed. Often the physiologically acceptable carrier is an aqueous pH buffered solution. Examples of physiologically acceptable carriers include buffers such as phosphate, citrate, and other organic acids; antioxidants including ascorbic acid; low molecular weight (less than about 10 residues) polypeptide; proteins, such as serum albumin, gelatin, or immunoglobulins; hydrophilic polymers such as polyvinylpyrrolidone; amino acids such as glycine, glutamine, asparagine, arginine or lysine; PATENT Attorney Docket No.: 50474-320WO2 Genentech Docket No.: P38318-WO monosaccharides, disaccharides, and other carbohydrates including glucose, mannose, or dextrins; chelating agents such as EDTA; sugar alcohols such as mannitol or sorbitol; salt-forming counterions such as sodium; and / or nonionic surfactants such as TWEEN™, polyethylene glycol (PEG), and PLURONICS™. The phrase “pharmaceutically acceptable” indicates that the substance or composition must be compatible chemically and / or toxicologically, with the other ingredients comprising a formulation, and / or the mammal being treated therewith. The term “pharmaceutical formulation” refers to a preparation which is in such form as to permit the biological activity of an active ingredient contained therein to be effective, and which contains no additional components which are unacceptably toxic to a subject to which the formulation would be administered. II. PROGNOSTIC METHODS AND ASSAYS FOR TIRAGOLUMAB PLUS ATEZOLIZUMAB A. CCL5, CXCR3, CCR7, and CXCR6 Methods of identifying individuals who may benefit from treatment In one aspect, the invention provides a method of identifying an individual having a non-small cell lung cancer (NSCLC) who may benefit from a treatment comprising atezolizumab and tiragolumab, the method comprising detecting an expression level of one or more of CCL5, CXCR3, CCR7, and CXCR6 (e.g., one, two, three, or all four of CCL5, CXCR3, CCR7, and CXCR6) in a sample from the individual, wherein an expression level of one or more of CCL5, CXCR3, CCR7, and CXCR6 that is at or above a reference expression level of CCL5, CXCR3, CCR7, or CXCR6 (e.g., an expression level of one, two, three, or all four of CCL5, CXCR3, CCR7, and CXCR6 that is at or above a reference expression level of CCL5, CXCR3, CCR7, or CXCR6) identifies the individual as one who may benefit from a treatment comprising atezolizumab and tiragolumab. For example, in one aspect, the invention provides a method of identifying an individual having a NSCLC who may benefit from a treatment comprising atezolizumab and tiragolumab, the method comprising detecting an expression level of CCL5 in a sample from the individual, wherein an expression level of CCL5 that is at or above a reference expression level of CCL5 identifies the individual as one who may benefit from a treatment comprising atezolizumab and tiragolumab. In another aspect, the invention provides a method of identifying an individual having a NSCLC who may benefit from a treatment comprising atezolizumab and tiragolumab, the method comprising detecting an expression level of CXCR3 in a sample from the individual, wherein an expression level of CXCR3 that is at or above a reference expression level of CXCR3 identifies the individual as one who may benefit from a treatment comprising atezolizumab and tiragolumab. In another aspect, the invention provides a method of identifying an individual having a NSCLC who may benefit from a treatment comprising atezolizumab and tiragolumab, the method comprising detecting an expression level of CCR7 in a sample from the individual, wherein an expression level of PATENT Attorney Docket No.: 50474-320WO2 Genentech Docket No.: P38318-WO CCR7 that is at or above a reference expression level of CCR7 identifies the individual as one who may benefit from a treatment comprising atezolizumab and tiragolumab. In another aspect, the invention provides a method of identifying an individual having a NSCLC who may benefit from a treatment comprising atezolizumab and tiragolumab, the method comprising detecting an expression level of CXCR6 in a sample from the individual, wherein an expression level of CXCR6 that is at or above a reference expression level of CXCR6 identifies the individual as one who may benefit from a treatment comprising atezolizumab and tiragolumab. In some aspects, the individual has an expression level of one or more of CCL5, CXCR3, CCR7, and CXCR6 in the sample that is at or above a reference expression level of CCL5, CXCR3, CCR7, or CXCR6, and the method further comprises administering to the individual an effective amount of atezolizumab and tiragolumab (e.g., an effective amount of atezolizumab and tiragolumab as described in Section III herein). Methods of selecting a therapy In another aspect, the invention provides a method of selecting a therapy for an individual having a NSCLC, the method comprising detecting an expression level of one or more of CCL5, CXCR3, CCR7, and CXCR6 (e.g., one, two, three, or all four of CCL5, CXCR3, CCR7, and CXCR6) in a sample from the individual, wherein an expression level of one or more of CCL5, CXCR3, CCR7, and CXCR6 that is at or above a reference expression level of CCL5, CXCR3, CCR7, or CXCR6 (e.g., an expression level of one, two, three, or all four of CCL5, CXCR3, CCR7, and CXCR6 that is at or above a reference expression level of CCL5, CXCR3, CCR7, or CXCR6) identifies the individual as one who may benefit from a treatment comprising atezolizumab and tiragolumab. For example, in one aspect, the invention provides a method of selecting a therapy for an individual having a NSCLC who may benefit from a treatment comprising atezolizumab and tiragolumab, the method comprising detecting an expression level of CCL5 in a sample from the individual, wherein an expression level of CCL5 that is at or above a reference expression level of CCL5 identifies the individual as one who may benefit from a treatment comprising atezolizumab and tiragolumab. In another aspect, the invention provides a method of selecting a therapy for an individual having a NSCLC who may benefit from a treatment comprising atezolizumab and tiragolumab, the method comprising detecting an expression level of CXCR3 in a sample from the individual, wherein an expression level of CXCR3 that is at or above a reference expression level of CXCR3 identifies the individual as one who may benefit from a treatment comprising atezolizumab and tiragolumab. In another aspect, the invention provides a method of selecting a therapy for an individual having a NSCLC who may benefit from a treatment comprising atezolizumab and tiragolumab, the method comprising detecting an expression level of CCR7 in a sample from the individual, wherein an expression level of CCR7 that is at or above a reference expression level of CCR7 identifies the individual as one who may benefit from a treatment comprising atezolizumab and tiragolumab. In another aspect, the invention provides a method of selecting a therapy for an individual having a NSCLC who may benefit from a treatment comprising atezolizumab and tiragolumab, the method comprising detecting an expression level of CXCR6 in a sample from the individual, wherein an PATENT Attorney Docket No.: 50474-320WO2 Genentech Docket No.: P38318-WO expression level of CXCR6 that is at or above a reference expression level of CXCR6 identifies the individual as one who may benefit from a treatment comprising atezolizumab and tiragolumab. In some aspects, the individual has an expression level of one or more of CCL5, CXCR3, CCR7, and CXCR6 in the sample that is at or above a reference expression level of CCL5, CXCR3, CCR7, or CXCR6, and the method further comprises administering to the individual an effective amount of atezolizumab and tiragolumab (e.g., an effective amount of atezolizumab and tiragolumab as described in Section III herein). Methods of treatment In another aspect, the invention provides a method of treating an individual having a NSCLC, the method comprising (a) detecting an expression level of one or more of CCL5, CXCR3, CCR7, and CXCR6 (e.g., one, two, three, or all four of CCL5, CXCR3, CCR7, and CXCR6) in a sample from the individual, wherein the expression level of one or more of CCL5, CXCR3, CCR7, and CXCR6 is at or above a reference expression level of CCL5, CXCR3, CCR7, or CXCR6 and thereby identifies the individual as one who may benefit from a treatment comprising atezolizumab and tiragolumab; and (b) administering an effective amount of atezolizumab and tiragolumab to the individual. For example, in one aspect, the invention provides a method of treating an individual having a NSCLC, the method comprising (a) detecting an expression level of CCL5 in a sample from the individual, wherein the expression level of CCL5 is at or above a reference expression level of CCL5 and thereby identifies the individual as one who may benefit from a treatment comprising atezolizumab and tiragolumab; and (b) administering an effective amount of atezolizumab and tiragolumab to the individual. In another aspect, the invention provides a method of treating an individual having a NSCLC, the method comprising (a) detecting an expression level of CXCR3 in a sample from the individual, wherein the expression level of CXCR3 is at or above a reference expression level of CXCR3 and thereby identifies the individual as one who may benefit from a treatment comprising atezolizumab and tiragolumab; and (b) administering an effective amount of atezolizumab and tiragolumab to the individual. In another aspect, the invention provides a method of treating an individual having a NSCLC, the method comprising (a) detecting an expression level of CCR7 in a sample from the individual, wherein the expression level of CCR7 is at or above a reference expression level of CCR7 and thereby identifies the individual as one who may benefit from a treatment comprising atezolizumab and tiragolumab; and (b) administering an effective amount of atezolizumab and tiragolumab to the individual. In another aspect, the invention provides a method of treating an individual having a NSCLC, the method comprising (a) detecting an expression level of CXCR6 in a sample from the individual, wherein the expression level of CXCR6 is at or above a reference expression level of CXCR6 and thereby identifies the individual as one who may benefit from a treatment comprising atezolizumab and tiragolumab; and (b) administering an effective amount of atezolizumab and tiragolumab to the individual. In another aspect, the invention provides a method of treating an individual having a NSCLC, the method comprising administering atezolizumab and tiragolumab to the individual, wherein the individual has been determined to have an expression level of one or more of CCL5, CXCR3, CCR7, and CXCR6 (e.g., an expression level of one, two, three, or all four of CCL5, CXCR3, CCR7, and CXCR6) that is at or PATENT Attorney Docket No.: 50474-320WO2 Genentech Docket No.: P38318-WO above a reference expression level of CCL5, CXCR3, CCR7, or CXCR6, thereby identifying the individual as one who may benefit from a treatment comprising atezolizumab and tiragolumab. For example, in one aspect, the invention provides a method of treating an individual having a NSCLC, the method comprising administering atezolizumab and tiragolumab to the individual, wherein the individual has been determined to have an expression level of CCL5 that is at or above a reference expression level of CCL5, thereby identifying the individual as one who may benefit from a treatment comprising atezolizumab and tiragolumab. In another aspect, the invention provides a method of treating an individual having a NSCLC, the method comprising administering atezolizumab and tiragolumab to the individual, wherein the individual has been determined to have an expression level of CXCR3 that is at or above a reference expression level of CXCR3, thereby identifying the individual as one who may benefit from a treatment comprising atezolizumab and tiragolumab. In another aspect, the invention provides a method of treating an individual having a NSCLC, the method comprising administering atezolizumab and tiragolumab to the individual, wherein the individual has been determined to have an expression level of CCR7 that is at or above a reference expression level of CCR7, thereby identifying the individual as one who may benefit from a treatment comprising atezolizumab and tiragolumab. In another aspect, the invention provides a method of treating an individual having a NSCLC, the method comprising administering atezolizumab and tiragolumab to the individual, wherein the individual has been determined to have an expression level of CXCR6 that is at or above a reference expression level of CXCR6, thereby identifying the individual as one who may benefit from a treatment comprising atezolizumab and tiragolumab. In another aspect, the invention provides use of atezolizumab and / or tiragolumab in the manufacture of a medicament for the treatment of an individual having a NSCLC, wherein the individual has been determined to have an expression level of one or more of CCL5, CXCR3, CCR7, and CXCR6 in a sample from the individual that is at or above a reference expression level of CCL5, CXCR3, CCR7, or CXCR6, thereby identifying the individual as one who may benefit from a treatment comprising atezolizumab and tiragolumab. In another aspect, the invention provides atezolizumab and / or tiragolumab for use in treating an individual having a NSCLC, wherein the individual has been determined to have an expression level of one or more of CCL5, CXCR3, CCR7, and CXCR6 in a sample from the individual that is at or above a reference expression level of CCL5, CXCR3, CCR7, or CXCR6, thereby identifying the individual as one who may benefit from a treatment comprising atezolizumab and tiragolumab. PATENT Attorney Docket No.: 50474-320WO2 Genentech Docket No.: P38318-WO Benefit An individual who benefits from receiving treatment with atezolizumab and tiragolumab may experience, for example, a delay or prevention in the occurrence or recurrence of NSCLC, alleviation of symptoms of the cancer, diminishment of any direct or indirect pathological consequences of the cancer, prevention of metastasis, decrease in the rate of disease progression, amelioration or palliation of the disease state, or remission or improved prognosis. In some aspects, the benefit achieved by the treatment comprising atezolizumab and tiragolumab is a clinical response, e.g., a complete response (CR) or a partial response (PR) (e.g., an individual treated by the method has an increased likelihood of achieving a CR or PR and / or the frequency of CR or PR is increased in the population of individuals treated according to the method). In some aspects, the individual has an expression level of one or more of CCL5, CXCR3, and CCR7 (e.g., an expression level of one, two, or all three of CCL5, CXCR3, and CCR7) in the sample that is at or above a reference expression level of CCL5, CXCR3, or CCR7 and the benefit is an increase in overall survival (OS) hazard ratio (HR) (e.g., an increase in the average OS HR of a population of individuals treated according to the method). In some aspects, the individual has an expression level of one or more of CCL5, CXCR3, and CXCR6 (e.g., an expression level of one, two, or all three of CCL5, CXCR3, and CXCR6) in the sample that is at or above a reference expression level of CCL5, CXCR3, or CXCR6 and the benefit is an increase in overall survival (OS) (e.g., an increase in the duration of OS experienced by an individual treated according to the method or an increase in the average OS of a population of individuals treated according to the method). An increased clinical response likelihood, OS HR, and / or OS may be determined by comparison to, e.g., an untreated reference individual and / or a reference population of individuals; a reference individual and / or a reference population of individuals who have received a control treatment, such as one or more previously approved treatments or marketed products for treatment of the cancer; and / or a reference individual and / or a reference population of individuals who have been treated with atezolizumab or tiragolumab as a monotherapy. In some aspects, the increased clinical response likelihood, OS HR, and / or OS is determined relative to a reference individual and / or a reference population of individuals having cancer that have been treated with a treatment comprising atezolizumab and tiragolumab, wherein the reference individual and / or each individual in the reference population has an expression level of each of CCL5, CXCR3, CCR7, and CXCR6 that is below a respective reference expression level. Reference expression levels are described herein and may be, for example, a median expression level of CCL5, CXCR3, CCR7, or CXCR6 in a reference population of individuals having a NSCLC. The skilled person is readily able to decide whether a given clinical outcome is improved in accordance with the invention. For example, "improved" in this context means that the clinical outcome resulting from the treatment of an individual having an expression level of one or more of CCL5, CXCR3, CCR7, and CXCR6 that is above a respective reference expression level with a treatment comprising atezolizumab and tiragolumab is at least 3% higher, at least 5% higher, at least 7% higher, at least 10% higher, at least 15% higher, at least 20% higher, at least 25% higher, at least 30% higher, at least 40% PATENT Attorney Docket No.: 50474-320WO2 Genentech Docket No.: P38318-WO higher, at least 50% higher, at least 75% higher, at least 100% higher, or at least 120% higher, as compared to the clinical outcome resulting from a comparator treatment as described above. For example, in some aspects, the duration of OS experienced by an individual treated according to the method or the average OS of a population of individuals treated according to the method is increased by at least 3%, at least 5%, at least 7%, at least 10%, at least 15%, at least 20%, at least 25%, at least 30%, at least 40%, at least 50%, at least 75%, at least 100%, or at least 120%. The time at which the clinical outcome / clinical endpoint is assessed can readily be determined by the skilled person. In principle, it is determined at a timepoint when the difference in the clinical outcome / clinical endpoint between the two treatments becomes evident. This time may, for example, be at least 1 month, at least 2 months, at least 3 months, at least 6 months, at least 12 months, at least 18 months, at least 24 months, at least 30 months, at least 36 months, at least 42 months, or at least 48 months after the beginning of the treatment. B. Gene signatures comprising CCL5, CXCR3, and CXCR6 Methods of identifying individuals who may benefit from treatment with atezolizumab and tiragolumab In one aspect, the invention provides a method of identifying an individual having a NSCLC who may benefit from a treatment comprising atezolizumab and tiragolumab, the method comprising detecting an expression level of each of CCL5, CXCR3, and CXCR6 in a sample from the individual and determining a gene signature score therefrom, wherein a gene signature score that is at or above a reference gene signature score identifies the individual as one who may benefit from a treatment comprising atezolizumab and tiragolumab. In some aspects, the individual has a gene signature score in the sample that is at or above a reference gene signature score, and the method further comprises administering to the individual an effective amount of atezolizumab and tiragolumab (e.g., an effective amount of atezolizumab and tiragolumab as described in Section III herein). In some aspects, the gene signature score is an average of the expression levels of CCL5, CXCR3, and CXCR6 in the sample from the individual. In other aspects, the method comprises further detecting the expression level of CCR7 in the sample from the individual, and the gene signature score is an average of the expression levels of CCL5, CXCR3, CXCR6, and CCR7 in the sample from the individual. Accordingly, in one aspect, the invention provides a method of identifying an individual having a NSCLC who may benefit from a treatment comprising atezolizumab and tiragolumab, the method comprising detecting an expression level of each of CCL5, CXCR3, CXCR6, and CCR7 in a sample from the individual and determining a gene signature score therefrom, wherein a gene signature score that is at or above a reference gene signature score identifies the individual as one who may benefit from a treatment comprising atezolizumab and tiragolumab. PATENT Attorney Docket No.: 50474-320WO2 Genentech Docket No.: P38318-WO Methods of identifying individuals who may benefit from treatment with atezolizumab In another aspect, the invention provides a method of identifying an individual having a NSCLC (e.g., a PD-L1-positive NSCLC, e.g., a NSCLC having a PD-L1 tumor proportion score (TPS) ≥1% as determined using the Ventana (SP263) PD-L1 IHC assay) who may benefit from a treatment comprising atezolizumab (e.g., atezolizumab monotherapy), the method comprising detecting an expression level of each of CCL5, CXCR3, and CXCR6 in a sample from the individual and determining a gene signature score therefrom, wherein a gene signature score that is at or above a reference gene signature score identifies the individual as one who may benefit from a treatment comprising atezolizumab. In some aspects, the individual has a gene signature score in the sample that is at or above a reference gene signature score, and the method further comprises administering to the individual an effective amount of atezolizumab (e.g., an effective amount of atezolizumab as described in Section III herein). In some aspects, the gene signature score is an average of the expression levels of CCL5, CXCR3, and CXCR6 in the sample from the individual. In other aspects, the method comprises further detecting the expression level of CCR7 in the sample from the individual, and the gene signature score is an average of the expression levels of CCL5, CXCR3, CXCR6, and CCR7 in the sample from the individual. Accordingly, in one aspect, the invention provides a method of identifying an individual having a NSCLC who may benefit from a treatment comprising atezolizumab (e.g., atezolizumab monotherapy), the method comprising detecting an expression level of each of CCL5, CXCR3, CXCR6, and CCR7 in a sample from the individual and determining a gene signature score therefrom, wherein a gene signature score that is at or above a reference gene signature score identifies the individual as one who may benefit from a treatment comprising atezolizumab. In some aspects, the individual has not previously been treated for NSCLC (e.g., has not previously been treated for Stage IV NSCLC). Methods of selecting a therapy for an individual who may benefit from treatment with atezolizumab and tiragolumab In another aspect, the invention provides a method for selecting a therapy for an individual having a NSCLC, the method comprising detecting an expression level of each of CCL5, CXCR3, and CXCR6 in a sample from the individual and determining a gene signature score therefrom, wherein a gene signature score that is at or above a reference gene signature score identifies the individual as one who may benefit from a treatment comprising atezolizumab and tiragolumab. In some aspects, the individual has a gene signature score in the sample that is at or above a reference gene signature score, and the method further comprises administering to the individual an effective amount of atezolizumab and tiragolumab (e.g., an effective amount of atezolizumab and tiragolumab as described in Section III herein). PATENT Attorney Docket No.: 50474-320WO2 Genentech Docket No.: P38318-WO In some aspects, the gene signature score is an average of the expression levels of CCL5, CXCR3, and CXCR6 in the sample from the individual. In other aspects, the method comprises further detecting the expression level of CCR7 in the sample from the individual, and the gene signature score is an average of the expression levels of CCL5, CXCR3, CXCR6, and CCR7 in the sample from the individual. Accordingly, in one aspect, the invention provides a method of selecting a therapy for an individual having a NSCLC, the method comprising detecting an expression level of each of CCL5, CXCR3, CXCR6, and CCR7 in a sample from the individual and determining a gene signature score therefrom, wherein a gene signature score that is at or above a reference gene signature score identifies the individual as one who may benefit from a treatment comprising atezolizumab and tiragolumab. Methods of selecting a therapy for an individual who may benefit from treatment with atezolizumab In another aspect, the invention provides a method for selecting a therapy for an individual having a NSCLC (e.g., a PD-L1-positive NSCLC, e.g., a NSCLC having a PD-L1 tumor proportion score (TPS) ≥1% as determined using the Ventana (SP263) PD-L1 IHC assay), the method comprising detecting an expression level of each of CCL5, CXCR3, and CXCR6 in a sample from the individual and determining a gene signature score therefrom, wherein a gene signature score that is at or above a reference gene signature score identifies the individual as one who may benefit from a treatment comprising atezolizumab (e.g., atezolizumab monotherapy). In some aspects, the individual has a gene signature score in the sample that is at or above a reference gene signature score, and the method further comprises administering to the individual an effective amount of atezolizumab (e.g., an effective amount of atezolizumab as described in Section III herein). In some aspects, the gene signature score is an average of the expression levels of CCL5, CXCR3, and CXCR6 in the sample from the individual. In other aspects, the method comprises further detecting the expression level of CCR7 in the sample from the individual, and the gene signature score is an average of the expression levels of CCL5, CXCR3, CXCR6, and CCR7 in the sample from the individual. Accordingly, in one aspect, the invention provides a method of selecting a therapy for an individual having a NSCLC, the method comprising detecting an expression level of each of CCL5, CXCR3, CXCR6, and CCR7 in a sample from the individual and determining a gene signature score therefrom, wherein a gene signature score that is at or above a reference gene signature score identifies the individual as one who may benefit from a treatment comprising atezolizumab (e.g., atezolizumab monotherapy). In some aspects, the individual has not previously been treated for NSCLC (e.g., has not previously been treated for Stage IV NSCLC). Methods of treatment comprising atezolizumab and tiragolumab In another aspect, the invention provides a method of treating an individual having a NSCLC, the method comprising (a) detecting an expression level of each of CCL5, CXCR3, and CXCR6 in a sample PATENT Attorney Docket No.: 50474-320WO2 Genentech Docket No.: P38318-WO from the individual and determining a gene signature score therefrom, wherein the gene signature score is at or above a reference gene signature score and thereby identifies the individual as one who may benefit from a treatment comprising atezolizumab and tiragolumab; and (b) administering an effective amount of atezolizumab and tiragolumab to the individual. In another aspect, the invention provides a method of treating an individual having a NSCLC, the method comprising administering atezolizumab and tiragolumab to the individual, wherein the individual has been determined to have a gene signature score that is at or above a reference gene signature score, thereby identifying the individual as one who may benefit from a treatment comprising atezolizumab and tiragolumab, and wherein the gene signature score is based on the expression level of each of CCL5, CXCR3, and CXCR6 detected in a sample from the individual. In some aspects, the gene signature score is an average of the expression levels of CCL5, CXCR3, and CXCR6 in the sample from the individual. In other aspects, the expression level of CCR7 has been detected in the sample from the individual, and the gene signature score is an average of the expression levels of CCL5, CXCR3, CXCR6, and CCR7 in the sample from the individual. Accordingly, in one aspect, the invention provides a method of treating an individual having a NSCLC, the method comprising (a) detecting an expression level of each of CCL5, CXCR3, CXCR6, and CCR7 in a sample from the individual and determining a gene signature score therefrom, wherein the gene signature score is at or above a reference gene signature score and thereby identifies the individual as one who may benefit from a treatment comprising atezolizumab and tiragolumab; and (b) administering an effective amount of atezolizumab and tiragolumab to the individual. In another aspect, the invention provides a method of treating an individual having a NSCLC, the method comprising administering atezolizumab and tiragolumab to the individual, wherein the individual has been determined to have a gene signature score that is at or above a reference gene signature score, thereby identifying the individual as one who may benefit from a treatment comprising atezolizumab and tiragolumab, and wherein the gene signature score is based on the expression level of each of CCL5, CXCR3, CXCR6, and CCR7 detected in a sample from the individual. In another aspect, the invention provides use of atezolizumab and / or tiragolumab in the manufacture of a medicament for the treatment of an individual having a NSCLC, wherein the individual has been determined to have a gene signature score that is at or above a reference gene signature score, thereby identifying the individual as one who may benefit from a treatment comprising atezolizumab and tiragolumab, wherein the gene signature score is based on the expression level of each of CCL5, CXCR3, and CXCR6 detected in a sample from the individual. In another aspect, the invention provides atezolizumab and / or tiragolumab for use in treating an individual having a NSCLC, wherein the individual has been determined to have a gene signature score that is at or above a reference gene signature score, thereby identifying the individual as one who may benefit from a treatment comprising atezolizumab and tiragolumab, wherein the gene signature score is based on the expression level of each of CCL5, CXCR3, and CXCR6 detected in a sample from the individual. PATENT Attorney Docket No.: 50474-320WO2 Genentech Docket No.: P38318-WO Methods of treatment comprising atezolizumab In another aspect, the invention provides a method of treating an individual having a NSCLC (e.g., a PD-L1-positive NSCLC, e.g., a NSCLC having a PD-L1 tumor proportion score (TPS) ≥1% as determined using the Ventana (SP263) PD-L1 IHC assay), the method comprising (a) detecting an expression level of each of CCL5, CXCR3, and CXCR6 in a sample from the individual and determining a gene signature score therefrom, wherein the gene signature score is at or above a reference gene signature score and thereby identifies the individual as one who may benefit from a treatment comprising atezolizumab (e.g., atezolizumab monotherapy); and (b) administering an effective amount of atezolizumab to the individual. In another aspect, the invention provides a method of treating an individual having a NSCLC (e.g., a PD-L1-positive NSCLC), the method comprising administering atezolizumab to the individual, wherein the individual has been determined to have a gene signature score that is at or above a reference gene signature score, thereby identifying the individual as one who may benefit from a treatment comprising atezolizumab (e.g., atezolizumab monotherapy), and wherein the gene signature score is based on the expression level of each of CCL5, CXCR3, and CXCR6 detected in a sample from the individual. In some aspects, the gene signature score is an average of the expression levels of CCL5, CXCR3, and CXCR6 in the sample from the individual. In other aspects, the expression level of CCR7 has been detected in the sample from the individual, and the gene signature score is an average of the expression levels of CCL5, CXCR3, CXCR6, and CCR7 in the sample from the individual. Accordingly, in one aspect, the invention provides a method of treating an individual having a NSCLC, the method comprising (a) detecting an expression level of each of CCL5, CXCR3, CXCR6, and CCR7 in a sample from the individual and determining a gene signature score therefrom, wherein the gene signature score is at or above a reference gene signature score and thereby identifies the individual as one who may benefit from a treatment comprising atezolizumab (e.g., atezolizumab monotherapy); and (b) administering an effective amount of atezolizumab to the individual. In another aspect, the invention provides a method of treating an individual having a NSCLC, the method comprising administering atezolizumab to the individual, wherein the individual has been determined to have a gene signature score that is at or above a reference gene signature score, thereby identifying the individual as one who may benefit from a treatment comprising atezolizumab (e.g., atezolizumab monotherapy), and wherein the gene signature score is based on the expression level of each of CCL5, CXCR3, CXCR6, and CCR7 detected in a sample from the individual. In some aspects, the individual has not previously been treated for NSCLC (e.g., has not previously been treated for Stage IV NSCLC). In another aspect, the invention provides use of atezolizumab in the manufacture of a medicament for the treatment of an individual having a NSCLC, wherein the individual has been determined to have a gene signature score that is at or above a reference gene signature score, thereby identifying the individual as one who may benefit from a treatment comprising atezolizumab, wherein the gene signature score is based on the expression level of each of CCL5, CXCR3, and CXCR6 detected in a sample from the individual. PATENT Attorney Docket No.: 50474-320WO2 Genentech Docket No.: P38318-WO In another aspect, the invention provides atezolizumab for use in treating an individual having a NSCLC, wherein the individual has been determined to have a gene signature score that is at or above a reference gene signature score, thereby identifying the individual as one who may benefit from a treatment comprising atezolizumab, wherein the gene signature score is based on the expression level of each of CCL5, CXCR3, and CXCR6 detected in a sample from the individual. Benefit of treatment comprising atezolizumab and tiragolumab In some aspects, the benefit achieved by the treatment comprising atezolizumab and tiragolumab is a clinical response, e.g., a complete response (CR) or a partial response (PR) (e.g., an individual treated by the method has an increased likelihood of achieving a CR or PR and / or the frequency of CR or PR is increased in the population of individuals treated according to the method). In some aspects, the benefit achieved by the treatment comprising atezolizumab and tiragolumab is an increase in overall survival (OS) hazard ratio (HR) (e.g., an increase in the average OS HR of a population of individuals treated according to the method). In some aspects, the benefit achieved by the treatment comprising atezolizumab and tiragolumab is an increase in overall survival (OS) (e.g., an increase in the duration of OS experienced by an individual treated according to the method or an increase in the average OS of a population of individuals treated according to the method). An increased clinical response likelihood, OS HR, and / or OS may be determined by comparison to, e.g., an untreated reference individual and / or a reference population of individuals; a reference individual and / or a reference population of individuals who have received a control treatment, such as one or more previously approved treatments or marketed products for treatment of the cancer; and / or a reference individual and / or a reference population of individuals who have been treated with atezolizumab or tiragolumab as a monotherapy. In some aspects, the increased clinical response likelihood, OS HR, and / or OS is determined relative to a reference individual and / or a reference population of individuals having cancer that have been treated with a treatment comprising atezolizumab and tiragolumab, wherein the reference individual and / or each individual in the reference population has a gene signature score is based on the expression level of (a) each of CCL5, CXCR3, and CXCR6 or (b) each of CCL5, CXCR3, CXCR6, and CCR7 that is below a respective reference gene signature score. The skilled person is readily able to decide whether a given clinical outcome is improved in accordance with the invention. For example, "improved" in this context means that the clinical outcome resulting from the treatment of an individual having a gene signature score is based on the expression level of (a) each of CCL5, CXCR3, and CXCR6 or (b) each of CCL5, CXCR3, CXCR6, and CCR7 that is above a respective reference expression level with a treatment comprising atezolizumab and tiragolumab is at least 3% higher, at least 5% higher, at least 7% higher, at least 10% higher, at least 15% higher, at least 20% higher, at least 25% higher, at least 30% higher, at least 40% higher, at least 50% higher, at least 75% higher, at least 100% higher, or at least 120% higher, as compared to the clinical outcome resulting from a comparator treatment as described above. For example, in some aspects, the duration of OS experienced by an individual treated according to the method or the average OS of a population of individuals treated according to the method is PATENT Attorney Docket No.: 50474-320WO2 Genentech Docket No.: P38318-WO increased by at least 3%, at least 5%, at least 7%, at least 10%, at least 15%, at least 20%, at least 25%, at least 30%, at least 40%, at least 50%, at least 75%, at least 100%, or at least 120%. The time at which the clinical outcome / clinical endpoint is assessed can readily be determined by the skilled person. In principle, it is determined at a timepoint when the difference in the clinical outcome / clinical endpoint between the two treatments becomes evident. This time may, for example, be at least 1 month, at least 2 months, at least 3 months, at least 6 months, at least 12 months, at least 18 months, at least 24 months, at least 30 months, at least 36 months, at least 42 months, or at least 48 months after the beginning of the treatment. Benefit of treatment comprising atezolizumab In some aspects, the benefit achieved by the treatment comprising atezolizumab (e.g., atezolizumab monotherapy) is an increase in overall survival (OS) (e.g., an increase in the duration of OS experienced by an individual treated according to the method or an increase in the average OS of a population of individuals treated according to the method). In some aspects, the benefit achieved by the treatment comprising atezolizumab (e.g., atezolizumab monotherapy) is an increase in progression-free survival (PFS) (e.g., an increase in the duration of PFS experienced by an individual treated according to the method or an increase in the average PFS of a population of individuals treated according to the method). An increased OS and / or PFS may be determined by comparison to, e.g., an untreated reference individual and / or a reference population of individuals; a reference individual and / or a reference population of individuals who have received a control treatment, such as one or more previously approved treatments or marketed products for treatment of the cancer. In some aspects, the increased OS and / or PFS is determined relative to a reference individual and / or a reference population of individuals having cancer that have been treated with a treatment comprising a PD-1 axis binding antagonist (e.g., atezolizumab), wherein the reference individual and / or each individual in the reference population has a gene signature score is based on the expression level of (a) each of CCL5, CXCR3, and CXCR6 or (b) each of CCL5, CXCR3, CXCR6, and CCR7 that is below a respective reference gene signature score. The skilled person is readily able to decide whether a given clinical outcome is improved in accordance with the invention. For example, "improved" in this context means that the clinical outcome resulting from the treatment of an individual having a gene signature score is based on the expression level of (a) each of CCL5, CXCR3, and CXCR6 or (b) each of CCL5, CXCR3, CXCR6, and CCR7 that is above a respective reference expression level with a treatment comprising atezolizumab and tiragolumab is at least 3% higher, at least 5% higher, at least 7% higher, at least 10% higher, at least 15% higher, at least 20% higher, at least 25% higher, at least 30% higher, at least 40% higher, at least 50% higher, at least 75% higher, at least 100% higher, or at least 120% higher, as compared to the clinical outcome resulting from a comparator treatment as described above. For example, in some aspects, the duration of OS experienced by an individual treated according to the method or the average OS of a population of individuals treated according to the method is PATENT Attorney Docket No.: 50474-320WO2 Genentech Docket No.: P38318-WO increased by at least 3%, at least 5%, at least 7%, at least 10%, at least 15%, at least 20%, at least 25%, at least 30%, at least 40%, at least 50%, at least 75%, at least 100%, or at least 120%. in some aspects, the duration of PFS experienced by an individual treated according to the method or the average PFS of a population of individuals treated according to the method is increased by at least 3%, at least 5%, at least 7%, at least 10%, at least 15%, at least 20%, at least 25%, at least 30%, at least 40%, at least 50%, at least 75%, at least 100%, or at least 120%. The time at which the clinical outcome / clinical endpoint is assessed can readily be determined by the skilled person. In principle, it is determined at a timepoint when the difference in the clinical outcome / clinical endpoint between the two treatments becomes evident. This time may, for example, be at least 1 month, at least 2 months, at least 3 months, at least 6 months, at least 12 months, at least 18 months, at least 24 months, at least 30 months, at least 36 months, at least 42 months, or at least 48 months after the beginning of the treatment. C. Ccr7.2, Ccr7.3, Cxcr3, Ccl5.1, Ifit, Mitotic Cytotox.2, and Cytotox.4 gene signatures Methods of identifying individuals who may benefit from treatment In another aspect, the invention provides a method of identifying an individual having a NSCLC who may benefit from a treatment comprising atezolizumab and tiragolumab, the method comprising: (a) detecting an expression level of at least two of STAT1, LEF1, IRGM, CCR7, SELL, RPS24, RPS27, GBP2, RPS29, RPS3A, RPS20, KLF2, RPLP1, RPL13, DAPL1, SMC6, RFLNB, and RPS4X (e.g., 2, 3, 4, 5, 6, 7, 8, 9, 10, 11, 12, 13, 14, 15, 16, 17, or all 18 of STAT1, LEF1, IRGM, CCR7, SELL, RPS24, RPS27, GBP2, RPS29, RPS3A, RPS20, KLF2, RPLP1, RPL13, DAPL1, SMC6, RFLNB, and RPS4X, e.g., each of STAT1, LEF1, IRGM, CCR7, SELL, RPS24, RPS27, GBP2, RPS29, RPS3A, RPS20, KLF2, RPLP1, RPL13, DAPL1, SMC6, RFLNB, and RPS4X) in a sample from the individual and determining a Ccr7.2 gene signature score therefrom; (b) detecting an expression level of at least two of DAPL1, CCR7, SMC4, RGCC, MXD4, CD8A, TCF7, ITGAE, RGS10, ZNRF1, CHD3, CD52, DDIT4, LEF1, IZUMO1R, INPP4B, and RFLNB (e.g., 2, 3, 4, 5, 6, 7, 8, 9, 10, 11, 12, 13, 14, 15, 16, or all 17 of DAPL1, CCR7, SMC4, RGCC, MXD4, CD8A, TCF7, ITGAE, RGS10, ZNRF1, CHD3, CD52, DDIT4, LEF1, IZUMO1R, INPP4B, and RFLNB, e.g., each of DAPL1, CCR7, SMC4, RGCC, MXD4, CD8A, TCF7, ITGAE, RGS10, ZNRF1, CHD3, CD52, DDIT4, LEF1, IZUMO1R, INPP4B, and RFLNB) in a sample from the individual and determining a Ccr7.3 gene signature score therefrom; (c) detecting an expression level of at least two of CXCR6, CKB, GIMAP5, ID2, LTB, FGL2, RAMP1, LYST, ASB2, IL2RB, CXCR3, SERINC3, INPP4B, ANXA1, XCL2, SOCS2, CD82, CD4, and GIMAP7 (e.g., 2, 3, 4, 5, 6, 7, 8, 9, 10, 11, 12, 13, 14, 15, 16, 17, 18, or all 19 of CXCR6, CKB, GIMAP5, ID2, LTB, FGL2, RAMP1, LYST, ASB2, IL2RB, CXCR3, SERINC3, INPP4B, ANXA1, XCL2, SOCS2, CD82, CD4, and GIMAP7, e.g., each of CXCR6, CKB, GIMAP5, ID2, LTB, FGL2, RAMP1, LYST, ASB2, IL2RB, CXCR3, SERINC3, INPP4B, ANXA1, XCL2, SOCS2, CD82, CD4, and GIMAP7) in a sample from the individual and determining a Cxcr3 gene signature score therefrom; (d) detecting an expression level of at least two CCL5, ITGB1, BTG1, GZMK, LTB, IL7R, ZFP36L2, ITGA4, TXNIP, SLAMF6, HCST, ETS1, CXCR3, MS4A4A, DGKA, and YPEL3 (e.g., at least 2, 3, 4, 5, 6, PATENT Attorney Docket No.: 50474-320WO2 Genentech Docket No.: P38318-WO 7, 8, 9, 10, 11, 12, 13, 14, 15, or all 16 of CCL5, ITGB1, BTG1, GZMK, LTB, IL7R, ZFP36L2, ITGA4, TXNIP, SLAMF6, HCST, ETS1, CXCR3, MS4A4A, DGKA, and YPEL3, e.g., of each of CCL5, ITGB1, BTG1, GZMK, LTB, IL7R, ZFP36L2, ITGA4, TXNIP, SLAMF6, HCST, ETS1, CXCR3, MS4A4A, DGKA, and YPEL3) in a sample from the individual and determining a Ccl5.1 gene signature score therefrom; (e) detecting an expression level of at least two of ISG15, IFIT1B, IFIT3, ISG20, IFI27L2, SAMHD1, ZBP1, SLFN5, IRF7, RTP4, USP18, PHF11, LGALS3BP, BST2, GBP2, IFITM3, STAT1, IFI16, and IFIH1 (e.g., 2, 3, 4, 5, 6, 7, 8, 9, 10, 11, 12, 13, 14, 15, 16, 17, 18, or all 19 of ISG15, IFIT1B, IFIT3, ISG20, IFI27L2, SAMHD1, ZBP1, SLFN5, STAT1, IFI16, and IFIH1, e.g., each of SLFN5, IRF7, RTP4, USP18, PHF11, a sample from the individual and determining an Ifit gene signature score therefrom; (f) detecting an expression level of at least two of HSP90AB1, PTMA, XCL2, ODC1, TNFRSF9, ITM2A, MYC, YBX3, HSPA5, GPX1, RPS12, TUBA1B, MCM6, TUBB, MCM3, TPI1, MCM5, DUT, and FTL (e.g., 2, 3, 4, 5, 6, 7, 8, 9, 10, 11, 12, 13, 14, 15, 16, 17, 18, or all 19 of HSP90AB1, PTMA, XCL2, ODC1, TNFRSF9, ITM2A, MYC, YBX3, HSPA5, GPX1, RPS12, TUBA1B, MCM6, TUBB, MCM3, TPI1, MCM5, DUT, and FTL, e.g., each of HSP90AB1, PTMA, XCL2, ODC1, TNFRSF9, ITM2A, MYC, YBX3, HSPA5, GPX1, RPS12, TUBA1B, MCM6, TUBB, MCM3, TPI1, MCM5, DUT, and FTL) in a sample from the individual and determining a Mitotic gene signature score therefrom; (g) detecting an expression level of at least two of HMGB2, TOP2A, MKI67, RRM2, PCLAF, TUBB, BIRC5, LMNB1, UBE2C, PTMA, STMN1, HMGN2, TUBA1B, LY6E, and DUT (e.g., 2, 3, 4, 5, 6, 7, 8, 9, 10, 11, 12, 13, 14, or all 15 of HMGB2, TOP2A, MKI67, RRM2, PCLAF, TUBB, BIRC5, LMNB1, UBE2C, PTMA, STMN1, HMGN2, TUBA1B, LY6E, and DUT, e.g., each of HMGB2, TOP2A, MKI67, RRM2, PCLAF, TUBB, BIRC5, LMNB1, UBE2C, PTMA, STMN1, HMGN2, TUBA1B, LY6E, and DUT) in a sample from the individual and determining a Cytotox.2 gene signature score therefrom; or (h) detecting an expression level of at least two of S100A6, NRN1, CXCR6, KLRC1, PDCD1, LGALS1, LAG3, ITGB1, ID2, LGALS3, NRGN, CST7, NKG7, S100A10, TNFRSF9, CD52, VIM, and IFITM2 (e.g., 2, 3, 4, 5, 6, 7, 8, 9, 10, 11, 12, 13, 14, 15, 16, 17, or all 18 of S100A6, NRN1, CXCR6, KLRC1, PDCD1, LGALS1, LAG3, ITGB1, ID2, LGALS3, NRGN, CST7, NKG7, S100A10, TNFRSF9, CD52, VIM, and IFITM2, e.g., each of S100A6, NRN1, CXCR6, KLRC1, PDCD1, LGALS1, LAG3, ITGB1, ID2, LGALS3, NRGN, CST7, NKG7, S100A10, TNFRSF9, CD52, VIM, and IFITM2) in a sample from the individual and determining a Cytotox.4 gene signature score therefrom; wherein (i) a Ccr7.2, Ccr7.3, Cxcr3, Ccl5.1, Ifit, or Mitotic gene signature score that is at or above a reference gene signature score identifies the individual as one who may benefit from a treatment comprising atezolizumab and tiragolumab, and (ii) a Cytotox.2 or Cytotox.4 gene signature score that is below a reference gene signature score identifies the individual as one who may benefit from a treatment comprising atezolizumab and tiragolumab. In some aspects, the individual has (i) a Ccr7.2, Ccr7.3, Cxcr3, Ccl5.1, Ifit, or Mitotic gene signature score in the sample that is at or above a reference gene signature score or (ii) a Cytotox.2 or Cytotox.4 gene signature score that is below a reference gene signature score, and the method further PATENT Attorney Docket No.: 50474-320WO2 Genentech Docket No.: P38318-WO comprises administering to the individual an effective amount of atezolizumab and tiragolumab (e.g., an effective amount of atezolizumab and tiragolumab as described in Section III herein). In some aspects, the gene signature score is an average of the expression levels of the members of the gene signature in the sample from the individual. In some aspects, the reference gene signature score is a pre-assigned gene signature score and / or a gene signature score in a reference population (e.g., a population of individuals having the NSCLC). In some aspects, the gene signature score in the reference population is the median Ccr7.2, Ccr7.3, Cxcr3, Ccl5.1, Ifit, Mitotic, Cytotox.2, or Cytotox.4 gene signature score in the reference population. Methods of selecting a therapy In another aspect, the invention provides a method for selecting a therapy for an individual having a NSCLC, the method comprising: (a) detecting an expression level of at least two of STAT1, LEF1, IRGM, CCR7, SELL, RPS24, RPS27, GBP2, RPS29, RPS3A, RPS20, KLF2, RPLP1, RPL13, DAPL1, SMC6, RFLNB, and RPS4X (e.g., 2, 3, 4, 5, 6, 7, 8, 9, 10, 11, 12, 13, 14, 15, 16, 17, or all 18 of STAT1, LEF1, IRGM, CCR7, SELL, RPS24, RPS27, GBP2, RPS29, RPS3A, RPS20, KLF2, RPLP1, RPL13, DAPL1, SMC6, RFLNB, and RPS4X, e.g., each of STAT1, LEF1, IRGM, CCR7, SELL, RPS24, RPS27, GBP2, RPS29, RPS3A, RPS20, KLF2, RPLP1, RPL13, DAPL1, SMC6, RFLNB, and RPS4X) in a sample from the individual and determining a Ccr7.2 gene signature score therefrom; (b) detecting an expression level of at least two of DAPL1, CCR7, SMC4, RGCC, MXD4, CD8A, TCF7, ITGAE, RGS10, ZNRF1, CHD3, CD52, DDIT4, LEF1, IZUMO1R, INPP4B, and RFLNB (e.g., 2, 3, 4, 5, 6, 7, 8, 9, 10, 11, 12, 13, 14, 15, 16, or all 17 of DAPL1, CCR7, SMC4, RGCC, MXD4, CD8A, TCF7, ITGAE, RGS10, ZNRF1, CHD3, CD52, DDIT4, LEF1, IZUMO1R, INPP4B, and RFLNB, e.g., each of DAPL1, CCR7, SMC4, RGCC, MXD4, CD8A, TCF7, ITGAE, RGS10, ZNRF1, CHD3, CD52, DDIT4, LEF1, IZUMO1R, INPP4B, and RFLNB) in a sample from the individual and determining a Ccr7.3 gene signature score therefrom; (c) detecting an expression level of at least two of CXCR6, CKB, GIMAP5, ID2, LTB, FGL2, RAMP1, LYST, ASB2, IL2RB, CXCR3, SERINC3, INPP4B, ANXA1, XCL2, SOCS2, CD82, CD4, and GIMAP7 (e.g., 2, 3, 4, 5, 6, 7, 8, 9, 10, 11, 12, 13, 14, 15, 16, 17, 18, or all 19 of CXCR6, CKB, GIMAP5, ID2, LTB, FGL2, RAMP1, LYST, ASB2, IL2RB, CXCR3, SERINC3, INPP4B, ANXA1, XCL2, SOCS2, CD82, CD4, and GIMAP7, e.g., each of CXCR6, CKB, GIMAP5, ID2, LTB, FGL2, RAMP1, LYST, ASB2, IL2RB, CXCR3, SERINC3, INPP4B, ANXA1, XCL2, SOCS2, CD82, CD4, and GIMAP7) in a sample from the individual and determining a Cxcr3 gene signature score therefrom; (d) detecting an expression level of at least two CCL5, ITGB1, BTG1, GZMK, LTB, IL7R, ZFP36L2, ITGA4, TXNIP, SLAMF6, HCST, ETS1, CXCR3, MS4A4A, DGKA, and YPEL3 (e.g., at least 2, 3, 4, 5, 6, 7, 8, 9, 10, 11, 12, 13, 14, 15, or all 16 of CCL5, ITGB1, BTG1, GZMK, LTB, IL7R, ZFP36L2, ITGA4, TXNIP, SLAMF6, HCST, ETS1, CXCR3, MS4A4A, DGKA, and YPEL3, e.g., of each of CCL5, ITGB1, BTG1, GZMK, LTB, IL7R, ZFP36L2, ITGA4, TXNIP, SLAMF6, HCST, ETS1, CXCR3, MS4A4A, DGKA, and YPEL3) in a sample from the individual and determining a Ccl5.1 gene signature score therefrom; PATENT Attorney Docket No.: 50474-320WO2 Genentech Docket No.: P38318-WO (e) detecting an expression level of at least two of ISG15, IFIT1B, IFIT3, ISG20, IFI27L2, SAMHD1, ZBP1, SLFN5, IRF7, RTP4, USP18, PHF11, LGALS3BP, BST2, GBP2, IFITM3, STAT1, IFI16, and IFIH1 (e.g., 2, 3, 4, 5, 6, 7, 8, 9, 10, 11, 12, 13, 14, 15, 16, 17, 18, or all 19 of ISG15, IFIT1B, IFIT3, ISG20, IFI27L2, SAMHD1, ZBP1, SLFN5, STAT1, IFI16, and IFIH1, e.g., each of SLFN5, IRF7, RTP4, USP18, PHF11, a sample from the individual and determining an Ifit gene signature score therefrom; (f) detecting an expression level of at least two of HSP90AB1, PTMA, XCL2, ODC1, TNFRSF9, ITM2A, MYC, YBX3, HSPA5, GPX1, RPS12, TUBA1B, MCM6, TUBB, MCM3, TPI1, MCM5, DUT, and FTL (e.g., 2, 3, 4, 5, 6, 7, 8, 9, 10, 11, 12, 13, 14, 15, 16, 17, 18, or all 19 of HSP90AB1, PTMA, XCL2, ODC1, TNFRSF9, ITM2A, MYC, YBX3, HSPA5, GPX1, RPS12, TUBA1B, MCM6, TUBB, MCM3, TPI1, MCM5, DUT, and FTL, e.g., each of HSP90AB1, PTMA, XCL2, ODC1, TNFRSF9, ITM2A, MYC, YBX3, HSPA5, GPX1, RPS12, TUBA1B, MCM6, TUBB, MCM3, TPI1, MCM5, DUT, and FTL) in a sample from the individual and determining a Mitotic gene signature score therefrom; (g) detecting an expression level of at least two of HMGB2, TOP2A, MKI67, RRM2, PCLAF, TUBB, BIRC5, LMNB1, UBE2C, PTMA, STMN1, HMGN2, TUBA1B, LY6E, and DUT (e.g., 2, 3, 4, 5, 6, 7, 8, 9, 10, 11, 12, 13, 14, or all 15 of HMGB2, TOP2A, MKI67, RRM2, PCLAF, TUBB, BIRC5, LMNB1, UBE2C, PTMA, STMN1, HMGN2, TUBA1B, LY6E, and DUT, e.g., each of HMGB2, TOP2A, MKI67, RRM2, PCLAF, TUBB, BIRC5, LMNB1, UBE2C, PTMA, STMN1, HMGN2, TUBA1B, LY6E, and DUT) in a sample from the individual and determining a Cytotox.2 gene signature score therefrom; or (h) detecting an expression level of at least two of S100A6, NRN1, CXCR6, KLRC1, PDCD1, LGALS1, LAG3, ITGB1, ID2, LGALS3, NRGN, CST7, NKG7, S100A10, TNFRSF9, CD52, VIM, and IFITM2 (e.g., 2, 3, 4, 5, 6, 7, 8, 9, 10, 11, 12, 13, 14, 15, 16, 17, or all 18 of S100A6, NRN1, CXCR6, KLRC1, PDCD1, LGALS1, LAG3, ITGB1, ID2, LGALS3, NRGN, CST7, NKG7, S100A10, TNFRSF9, CD52, VIM, and IFITM2, e.g., each of S100A6, NRN1, CXCR6, KLRC1, PDCD1, LGALS1, LAG3, ITGB1, ID2, LGALS3, NRGN, CST7, NKG7, S100A10, TNFRSF9, CD52, VIM, and IFITM2) in a sample from the individual and determining a Cytotox.4 gene signature score therefrom; wherein (i) a Ccr7.2, Ccr7.3, Cxcr3, Ccl5.1, Ifit, or Mitotic gene signature score that is at or above a reference gene signature score identifies the individual as one who may benefit from a treatment comprising atezolizumab and tiragolumab, and (ii) a Cytotox.2 or Cytotox.4 gene signature score that is below a reference gene signature score identifies the individual as one who may benefit from a treatment comprising atezolizumab and tiragolumab. In some aspects, the individual has (i) a Ccr7.2, Ccr7.3, Cxcr3, Ccl5.1, Ifit, or Mitotic gene signature score in the sample that is at or above a reference gene signature score or (ii) a Cytotox.2 or Cytotox.4 gene signature score that is below a reference gene signature score, and the method further comprises administering to the individual an effective amount of atezolizumab and tiragolumab (e.g., an effective amount of atezolizumab and tiragolumab as described in Section III herein). In some aspects, the gene signature score is an average of the expression levels of the members of the gene signature in the sample from the individual. PATENT Attorney Docket No.: 50474-320WO2 Genentech Docket No.: P38318-WO In some aspects, the reference gene signature score is a pre-assigned gene signature score and / or a gene signature score in a reference population (e.g., a population of individuals having the NSCLC). In some aspects, the gene signature score in the reference population is the median Ccr7.2, Ccr7.3, Cxcr3, Ccl5.1, Ifit, Mitotic, Cytotox.2, or Cytotox.4 gene signature score in the reference population. Methods of treatment In another aspect, the invention provides a method of treating an individual having a NSCLC, the method comprising: (i) (a) detecting an expression level of at least two of STAT1, LEF1, IRGM, CCR7, SELL, RPS24, RPS27, GBP2, RPS29, RPS3A, RPS20, KLF2, RPLP1, RPL13, DAPL1, SMC6, RFLNB, and RPS4X (e.g., 2, 3, 4, 5, 6, 7, 8, 9, 10, 11, 12, 13, 14, 15, 16, 17, or all 18 of STAT1, LEF1, IRGM, CCR7, SELL, RPS24, RPS27, GBP2, RPS29, RPS3A, RPS20, KLF2, RPLP1, RPL13, DAPL1, SMC6, RFLNB, and RPS4X, e.g., each of STAT1, LEF1, IRGM, CCR7, SELL, RPS24, RPS27, GBP2, RPS29, RPS3A, RPS20, KLF2, RPLP1, RPL13, DAPL1, SMC6, RFLNB, and RPS4X) in a sample from the individual and determining a Ccr7.2 gene signature score therefrom, wherein the gene signature score is at or above a reference gene signature score and thereby identifies the individual as one who may benefit from a treatment comprising atezolizumab and tiragolumab; (b) detecting an expression level of at least two of DAPL1, CCR7, SMC4, RGCC, MXD4, CD8A, TCF7, ITGAE, RGS10, ZNRF1, CHD3, CD52, DDIT4, LEF1, IZUMO1R, INPP4B, and RFLNB (e.g., 2, 3, 4, 5, 6, 7, 8, 9, 10, 11, 12, 13, 14, 15, 16, or all 17 of DAPL1, CCR7, SMC4, RGCC, MXD4, CD8A, TCF7, ITGAE, RGS10, ZNRF1, CHD3, CD52, DDIT4, LEF1, IZUMO1R, INPP4B, and RFLNB, e.g., each of DAPL1, CCR7, SMC4, RGCC, MXD4, CD8A, TCF7, ITGAE, RGS10, ZNRF1, CHD3, CD52, DDIT4, LEF1, IZUMO1R, INPP4B, and RFLNB) in a sample from the individual and determining a Ccr7.3 gene signature score therefrom, wherein the gene signature score is at or above a reference gene signature score and thereby identifies the individual as one who may benefit from a treatment comprising atezolizumab and tiragolumab; (c) detecting an expression level of at least two of CXCR6, CKB, GIMAP5, ID2, LTB, FGL2, RAMP1, LYST, ASB2, IL2RB, CXCR3, SERINC3, INPP4B, ANXA1, XCL2, SOCS2, CD82, CD4, and GIMAP7 (e.g., 2, 3, 4, 5, 6, 7, 8, 9, 10, 11, 12, 13, 14, 15, 16, 17, 18, or all 19 of CXCR6, CKB, GIMAP5, ID2, LTB, FGL2, RAMP1, LYST, ASB2, IL2RB, CXCR3, SERINC3, INPP4B, ANXA1, XCL2, SOCS2, CD82, CD4, and GIMAP7, e.g., each of CXCR6, CKB, GIMAP5, ID2, LTB, FGL2, RAMP1, LYST, ASB2, IL2RB, CXCR3, SERINC3, INPP4B, ANXA1, XCL2, SOCS2, CD82, CD4, and GIMAP7) in a sample from the individual and determining a Cxcr3 gene signature score therefrom, wherein the gene signature score is at or above a reference gene signature score and thereby identifies the individual as one who may benefit from a treatment comprising atezolizumab and tiragolumab; (d) detecting an expression level of at least two CCL5, ITGB1, BTG1, GZMK, LTB, IL7R, ZFP36L2, ITGA4, TXNIP, SLAMF6, HCST, ETS1, CXCR3, MS4A4A, DGKA, and YPEL3 (e.g., at least 2, 3, 4, 5, 6, 7, 8, 9, 10, 11, 12, 13, 14, 15, or all 16 of CCL5, ITGB1, BTG1, GZMK, LTB, IL7R, ZFP36L2, ITGA4, PATENT Attorney Docket No.: 50474-320WO2 Genentech Docket No.: P38318-WO TXNIP, SLAMF6, HCST, ETS1, CXCR3, MS4A4A, DGKA, and YPEL3, e.g., of each of CCL5, ITGB1, BTG1, GZMK, LTB, IL7R, ZFP36L2, ITGA4, TXNIP, SLAMF6, HCST, ETS1, CXCR3, MS4A4A, DGKA, and YPEL3) in a sample from the individual and determining a Ccl5.1 gene signature score therefrom, wherein the gene signature score is at or above a reference gene signature score and thereby identifies the individual as one who may benefit from a treatment comprising atezolizumab and tiragolumab; (e) detecting an expression level of at least two of ISG15, IFIT1B, IFIT3, ISG20, IFI27L2, SAMHD1, ZBP1, SLFN5, IRF7, RTP4, USP18, PHF11, LGALS3BP, BST2, GBP2, IFITM3, STAT1, IFI16, and IFIH1 (e.g., 2, 3, 4, 5, 6, 7, 8, 9, 10, 11, 12, 13, 14, 15, 16, 17, 18, or all 19 of ISG15, IFIT1B, IFIT3, ISG20, IFI27L2, SAMHD1, ZBP1, SLFN5, STAT1, IFI16, and IFIH1, e.g., each of SLFN5, IRF7, RTP4, USP18, PHF11, a sample from the individual and determining an Ifit gene signature score therefrom, wherein the gene signature score is at or above a reference gene signature score and thereby identifies the individual as one who may benefit from a treatment comprising atezolizumab and tiragolumab; (f) detecting an expression level of at least two of HSP90AB1, PTMA, XCL2, ODC1, TNFRSF9, ITM2A, MYC, YBX3, HSPA5, GPX1, RPS12, TUBA1B, MCM6, TUBB, MCM3, TPI1, MCM5, DUT, and FTL (e.g., 2, 3, 4, 5, 6, 7, 8, 9, 10, 11, 12, 13, 14, 15, 16, 17, 18, or all 19 of HSP90AB1, PTMA, XCL2, ODC1, TNFRSF9, ITM2A, MYC, YBX3, HSPA5, GPX1, RPS12, TUBA1B, MCM6, TUBB, MCM3, TPI1, MCM5, DUT, and FTL, e.g., each of HSP90AB1, PTMA, XCL2, ODC1, TNFRSF9, ITM2A, MYC, YBX3, HSPA5, GPX1, RPS12, TUBA1B, MCM6, TUBB, MCM3, TPI1, MCM5, DUT, and FTL) in a sample from the individual and determining a Mitotic gene signature score therefrom, wherein the gene signature score is at or above a reference gene signature score and thereby identifies the individual as one who may benefit from a treatment comprising atezolizumab and tiragolumab; (g) detecting an expression level of at least two of HMGB2, TOP2A, MKI67, RRM2, PCLAF, TUBB, BIRC5, LMNB1, UBE2C, PTMA, STMN1, HMGN2, TUBA1B, LY6E, and DUT (e.g., 2, 3, 4, 5, 6, 7, 8, 9, 10, 11, 12, 13, 14, or all 15 of HMGB2, TOP2A, MKI67, RRM2, PCLAF, TUBB, BIRC5, LMNB1, UBE2C, PTMA, STMN1, HMGN2, TUBA1B, LY6E, and DUT, e.g., each of HMGB2, TOP2A, MKI67, RRM2, PCLAF, TUBB, BIRC5, LMNB1, UBE2C, PTMA, STMN1, HMGN2, TUBA1B, LY6E, and DUT) in a sample from the individual and determining a Cytotox.2 gene signature score therefrom, wherein the gene signature score is below a reference gene signature score and thereby identifies the individual as one who may benefit from a treatment comprising atezolizumab and tiragolumab; or (h) detecting an expression level of at least two of S100A6, NRN1, CXCR6, KLRC1, PDCD1, LGALS1, LAG3, ITGB1, ID2, LGALS3, NRGN, CST7, NKG7, S100A10, TNFRSF9, CD52, VIM, and IFITM2 (e.g., 2, 3, 4, 5, 6, 7, 8, 9, 10, 11, 12, 13, 14, 15, 16, 17, or all 18 of S100A6, NRN1, CXCR6, KLRC1, PDCD1, LGALS1, LAG3, ITGB1, ID2, LGALS3, NRGN, CST7, NKG7, S100A10, TNFRSF9, CD52, VIM, and IFITM2, e.g., each of S100A6, NRN1, CXCR6, KLRC1, PDCD1, LGALS1, LAG3, ITGB1, ID2, LGALS3, NRGN, CST7, NKG7, S100A10, TNFRSF9, CD52, VIM, and IFITM2) in a sample from the individual and determining a Cytotox.4 gene signature score therefrom; and (ii) administering an effective amount of atezolizumab and tiragolumab to the individual. PATENT Attorney Docket No.: 50474-320WO2 Genentech Docket No.: P38318-WO In another aspect, the invention provides a method of treating an individual having a NSCLC, the method comprising administering atezolizumab and tiragolumab to the individual, wherein the individual has been determined to have: (a) a Ccr7.2 gene signature score based on an expression level at least two of STAT1, LEF1, IRGM, CCR7, SELL, RPS24, RPS27, GBP2, RPS29, RPS3A, RPS20, KLF2, RPLP1, RPL13, DAPL1, SMC6, RFLNB, and RPS4X (e.g., 2, 3, 4, 5, 6, 7, 8, 9, 10, 11, 12, 13, 14, 15, 16, 17, or all 18 of STAT1, LEF1, IRGM, CCR7, SELL, RPS24, RPS27, GBP2, RPS29, RPS3A, RPS20, KLF2, RPLP1, RPL13, DAPL1, SMC6, RFLNB, and RPS4X, e.g., each of STAT1, LEF1, IRGM, CCR7, SELL, RPS24, RPS27, GBP2, RPS29, RPS3A, RPS20, KLF2, RPLP1, RPL13, DAPL1, SMC6, RFLNB, and RPS4X) in a sample from the individual that is at or above a reference Ccr7.2 gene signature score; (b) a Ccr7.3 gene signature based on an expression level of at least two of DAPL1, CCR7, SMC4, RGCC, MXD4, CD8A, TCF7, ITGAE, RGS10, ZNRF1, CHD3, CD52, DDIT4, LEF1, IZUMO1R, INPP4B, and RFLNB (e.g., 2, 3, 4, 5, 6, 7, 8, 9, 10, 11, 12, 13, 14, 15, 16, or all 17 of DAPL1, CCR7, SMC4, RGCC, MXD4, CD8A, TCF7, ITGAE, RGS10, ZNRF1, CHD3, CD52, DDIT4, LEF1, IZUMO1R, INPP4B, and RFLNB, e.g., each of DAPL1, CCR7, SMC4, RGCC, MXD4, CD8A, TCF7, ITGAE, RGS10, ZNRF1, CHD3, CD52, DDIT4, LEF1, IZUMO1R, INPP4B, and RFLNB) in a sample from the individual that is at or above a reference Ccr7.3 gene signature score; (c) a Cxcr3 gene signature score based on an expression level at least two of CXCR6, CKB, GIMAP5, ID2, LTB, FGL2, RAMP1, LYST, ASB2, IL2RB, CXCR3, SERINC3, INPP4B, ANXA1, XCL2, SOCS2, CD82, CD4, and GIMAP7 (e.g., 2, 3, 4, 5, 6, 7, 8, 9, 10, 11, 12, 13, 14, 15, 16, 17, 18, or all 19 of CXCR6, CKB, GIMAP5, ID2, LTB, FGL2, RAMP1, LYST, ASB2, IL2RB, CXCR3, SERINC3, INPP4B, ANXA1, XCL2, SOCS2, CD82, CD4, and GIMAP7, e.g., each of CXCR6, CKB, GIMAP5, ID2, LTB, FGL2, RAMP1, LYST, ASB2, IL2RB, CXCR3, SERINC3, INPP4B, ANXA1, XCL2, SOCS2, CD82, CD4, and GIMAP7) in a sample from the individual that is at or above a reference Cxcr3 gene signature score; (d) a Ccl5.1 gene signature score based on an expression level of at least two of CCL5, ITGB1, BTG1, GZMK, LTB, IL7R, ZFP36L2, ITGA4, TXNIP, SLAMF6, HCST, ETS1, CXCR3, MS4A4A, DGKA, and YPEL3 (e.g., at least 2, 3, 4, 5, 6, 7, 8, 9, 10, 11, 12, 13, 14, 15, or all 16 of CCL5, ITGB1, BTG1, GZMK, LTB, IL7R, ZFP36L2, ITGA4, TXNIP, SLAMF6, HCST, ETS1, CXCR3, MS4A4A, DGKA, and YPEL3, e.g., of each of CCL5, ITGB1, BTG1, GZMK, LTB, IL7R, ZFP36L2, ITGA4, TXNIP, SLAMF6, HCST, ETS1, CXCR3, MS4A4A, DGKA, and YPEL3) in a sample from the individual that is at or above a reference Ccl5.1 gene signature score; (e) an Ifit gene signature score based on an expression level of at least two of ISG15, IFIT1B, IFIT3, STAT1, IFI16, and IFIH1) in a sample from the individual that is at or above a reference Ifit gene signature score; PATENT Attorney Docket No.: 50474-320WO2 Genentech Docket No.: P38318-WO (f) a Mitotic gene signature score based on an expression level of at least two of HSP90AB1, PTMA, XCL2, ODC1, TNFRSF9, ITM2A, MYC, YBX3, HSPA5, GPX1, RPS12, TUBA1B, MCM6, TUBB, MCM3, TPI1, MCM5, DUT, and FTL (e.g., 2, 3, 4, 5, 6, 7, 8, 9, 10, 11, 12, 13, 14, 15, 16, 17, 18, or all 19 of HSP90AB1, PTMA, XCL2, ODC1, TNFRSF9, ITM2A, MYC, YBX3, HSPA5, GPX1, RPS12, TUBA1B, MCM6, TUBB, MCM3, TPI1, MCM5, DUT, and FTL, e.g., each of HSP90AB1, PTMA, XCL2, ODC1, TNFRSF9, ITM2A, MYC, YBX3, HSPA5, GPX1, RPS12, TUBA1B, MCM6, TUBB, MCM3, TPI1, MCM5, DUT, and FTL) in a sample from the individual that is at or above a reference Mitotic gene signature score; (g) a Cytotox.2 gene signature score based on an expression level of at least two of HMGB2, TOP2A, MKI67, RRM2, PCLAF, TUBB, BIRC5, LMNB1, UBE2C, PTMA, STMN1, HMGN2, TUBA1B, LY6E, and DUT (e.g., 2, 3, 4, 5, 6, 7, 8, 9, 10, 11, 12, 13, 14, or all 15 of HMGB2, TOP2A, MKI67, RRM2, PCLAF, TUBB, BIRC5, LMNB1, UBE2C, PTMA, STMN1, HMGN2, TUBA1B, LY6E, and DUT, e.g., each of HMGB2, TOP2A, MKI67, RRM2, PCLAF, TUBB, BIRC5, LMNB1, UBE2C, PTMA, STMN1, HMGN2, TUBA1B, LY6E, and DUT) in a sample from the individual that is below a reference Cytotox.2 gene signature score; or (h) a Cytotox.4 gene signature score based on an expression level of at least two of S100A6, NRN1, CXCR6, KLRC1, PDCD1, LGALS1, LAG3, ITGB1, ID2, LGALS3, NRGN, CST7, NKG7, S100A10, TNFRSF9, CD52, VIM, and IFITM2 (e.g., 2, 3, 4, 5, 6, 7, 8, 9, 10, 11, 12, 13, 14, 15, 16, 17, or all 18 of S100A6, NRN1, CXCR6, KLRC1, PDCD1, LGALS1, LAG3, ITGB1, ID2, LGALS3, NRGN, CST7, NKG7, S100A10, TNFRSF9, CD52, VIM, and IFITM2, e.g., each of S100A6, NRN1, CXCR6, KLRC1, PDCD1, LGALS1, LAG3, ITGB1, ID2, LGALS3, NRGN, CST7, NKG7, S100A10, TNFRSF9, CD52, VIM, and IFITM2) in a sample from the individual that is below a reference Cytotox.4 gene signature score; thereby identifying the individual as one who may benefit from a treatment comprising atezolizumab and tiragolumab. In some aspects, the gene signature score is an average of the expression levels of the members of the gene signature in the sample from the individual. In some aspects, the reference gene signature score is a pre-assigned gene signature score and / or a gene signature score in a reference population (e.g., a population of individuals having the NSCLC). In some aspects, the gene signature score in the reference population is the median Ccr7.2, Ccr7.3, Cxcr3, Ccl5.1, Ifit, Mitotic, Cytotox.2, or Cytotox.4 gene signature score in the reference population. In another aspect, the invention provides use of atezolizumab and / or tiragolumab in the manufacture of a medicament for the treatment of an individual having a NSCLC, wherein the individual has been determined to have: PATENT Attorney Docket No.: 50474-320WO2 Genentech Docket No.: P38318-WO (i) (a) a Ccr7.2 gene signature score that is at or above a reference gene signature score, thereby identifying the individual as one who may benefit from a treatment comprising atezolizumab and tiragolumab, wherein the gene signature score is based on the expression level of each of STAT1, LEF1, IRGM, CCR7, SELL, RPS24, RPS27, GBP2, RPS29, RPS3A, RPS20, KLF2, RPLP1, RPL13, DAPL1, SMC6, RFLNB, and RPS4X detected in a sample from the individual; (b) a Ccr7.3 gene signature score that is at or above a reference gene signature score, thereby identifying the individual as one who may benefit from a treatment comprising atezolizumab and tiragolumab, wherein the gene signature score is based on the expression level of each of DAPL1, CCR7, SMC4, RGCC, MXD4, CD8A, TCF7, ITGAE, RGS10, ZNRF1, CHD3, CD52, DDIT4, LEF1, IZUMO1R, INPP4B, and RFLNB detected in a sample from the individual; (c) a Cxcr3 gene signature score that is at or above a reference gene signature score, thereby identifying the individual as one who may benefit from a treatment comprising atezolizumab and tiragolumab, wherein the gene signature score is based on the expression level of each of CXCR6, CKB, GIMAP5, ID2, LTB, FGL2, RAMP1, LYST, ASB2, IL2RB, CXCR3, SERINC3, INPP4B, ANXA1, XCL2, SOCS2, CD82, CD4, and GIMAP7 detected in a sample from the individual; (d) a Ccl5.1 gene signature score that is at or above a reference gene signature score, thereby identifying the individual as one who may benefit from a treatment comprising atezolizumab and tiragolumab, wherein the gene signature score is based on the expression level of each of CCL5, ITGB1, BTG1, GZMK, LTB, IL7R, ZFP36L2, ITGA4, TXNIP, SLAMF6, HCST, ETS1, CXCR3, MS4A4A, DGKA, and YPEL3 detected in a sample from the individual; (e) an Ifit gene signature score that is at or above a reference gene signature score, thereby identifying the individual as one who may benefit from a treatment comprising atezolizumab and tiragolumab, wherein the gene signature score is based on the expression level of each of ISG15, IFIT1B, IFIT3, ISG20, IFI27L2, SAMHD1, ZBP1, SLFN5, IRF7, RTP4, USP18, PHF11, LGALS3BP, BST2, GBP2, IFITM3, STAT1, IFI16, and IFIH1 detected in a sample from the individual; (f) a Mitotic gene signature score that is at or above a reference gene signature score, thereby identifying the individual as one who may benefit from a treatment comprising atezolizumab and tiragolumab, wherein the gene signature score is based on the expression level of each of HSP90AB1, PTMA, XCL2, ODC1, TNFRSF9, ITM2A, MYC, YBX3, HSPA5, GPX1, RPS12, TUBA1B, MCM6, TUBB, MCM3, TPI1, MCM5, DUT, and FTL detected in a sample from the individual; (g) a Cytotox.2 gene signature score that is below a reference gene signature score, thereby identifying the individual as one who may benefit from a treatment comprising atezolizumab and tiragolumab, wherein the gene signature score is based on the expression level of each of HMGB2, TOP2A, MKI67, RRM2, PCLAF, TUBB, BIRC5, LMNB1, UBE2C, PTMA, STMN1, HMGN2, TUBA1B, LY6E, and DUT detected in a sample from the individual; or (h) a Cytotox.4 gene signature score that is below a reference gene signature score, thereby identifying the individual as one who may benefit from a treatment comprising atezolizumab and tiragolumab, wherein the gene signature score is based on the expression level of each of S100A6, PATENT Attorney Docket No.: 50474-320WO2 Genentech Docket No.: P38318-WO NRN1, CXCR6, KLRC1, PDCD1, LGALS1, LAG3, ITGB1, ID2, LGALS3, NRGN, CST7, NKG7, S100A10, TNFRSF9, CD52, VIM, and IFITM2 detected in a sample from the individual. In another aspect, the invention provides atezolizumab and / or tiragolumab for use in treating an individual having a NSCLC, wherein the individual has been determined to have: (i) (a) a Ccr7.2 gene signature score that is at or above a reference gene signature score, thereby identifying the individual as one who may benefit from a treatment comprising atezolizumab and tiragolumab, wherein the gene signature score is based on the expression level of each of STAT1, LEF1, IRGM, CCR7, SELL, RPS24, RPS27, GBP2, RPS29, RPS3A, RPS20, KLF2, RPLP1, RPL13, DAPL1, SMC6, RFLNB, and RPS4X detected in a sample from the individual; (b) a Ccr7.3 gene signature score that is at or above a reference gene signature score, thereby identifying the individual as one who may benefit from a treatment comprising atezolizumab and tiragolumab, wherein the gene signature score is based on the expression level of each of DAPL1, CCR7, SMC4, RGCC, MXD4, CD8A, TCF7, ITGAE, RGS10, ZNRF1, CHD3, CD52, DDIT4, LEF1, IZUMO1R, INPP4B, and RFLNB detected in a sample from the individual; (c) a Cxcr3 gene signature score that is at or above a reference gene signature score, thereby identifying the individual as one who may benefit from a treatment comprising atezolizumab and tiragolumab, wherein the gene signature score is based on the expression level of each of CXCR6, CKB, GIMAP5, ID2, LTB, FGL2, RAMP1, LYST, ASB2, IL2RB, CXCR3, SERINC3, INPP4B, ANXA1, XCL2, SOCS2, CD82, CD4, and GIMAP7 detected in a sample from the individual; (d) a Ccl5.1 gene signature score that is at or above a reference gene signature score, thereby identifying the individual as one who may benefit from a treatment comprising atezolizumab and tiragolumab, wherein the gene signature score is based on the expression level of each of CCL5, ITGB1, BTG1, GZMK, LTB, IL7R, ZFP36L2, ITGA4, TXNIP, SLAMF6, HCST, ETS1, CXCR3, MS4A4A, DGKA, and YPEL3 detected in a sample from the individual; (e) an Ifit gene signature score that is at or above a reference gene signature score, thereby identifying the individual as one who may benefit from a treatment comprising atezolizumab and tiragolumab, wherein the gene signature score is based on the expression level of each of ISG15, IFIT1B, IFIT3, ISG20, IFI27L2, SAMHD1, ZBP1, SLFN5, IRF7, RTP4, USP18, PHF11, LGALS3BP, BST2, GBP2, IFITM3, STAT1, IFI16, and IFIH1 detected in a sample from the individual; (f) a Mitotic gene signature score that is at or above a reference gene signature score, thereby identifying the individual as one who may benefit from a treatment comprising atezolizumab and tiragolumab, wherein the gene signature score is based on the expression level of each of HSP90AB1, PTMA, XCL2, ODC1, TNFRSF9, ITM2A, MYC, YBX3, HSPA5, GPX1, RPS12, TUBA1B, MCM6, TUBB, MCM3, TPI1, MCM5, DUT, and FTL detected in a sample from the individual; (g) a Cytotox.2 gene signature score that is below a reference gene signature score, thereby identifying the individual as one who may benefit from a treatment comprising atezolizumab and tiragolumab, wherein the gene signature score is based on the expression level of each of HMGB2, TOP2A, MKI67, RRM2, PCLAF, TUBB, BIRC5, LMNB1, UBE2C, PTMA, STMN1, HMGN2, TUBA1B, LY6E, and DUT detected in a sample from the individual; or PATENT Attorney Docket No.: 50474-320WO2 Genentech Docket No.: P38318-WO (h) a Cytotox.4 gene signature score that is below a reference gene signature score, thereby identifying the individual as one who may benefit from a treatment comprising atezolizumab and tiragolumab, wherein the gene signature score is based on the expression level of each of S100A6, NRN1, CXCR6, KLRC1, PDCD1, LGALS1, LAG3, ITGB1, ID2, LGALS3, NRGN, CST7, NKG7, S100A10, TNFRSF9, CD52, VIM, and IFITM2 detected in a sample from the individual. Benefit In some aspects, the individual has a Ccr7.3, Cxcr3, or Ccl5.1 gene signature score in the sample that is at or above a reference gene signature score and the benefit achieved by the treatment comprising atezolizumab and tiragolumab is a clinical response, e.g., a complete response (CR) or a partial response (PR) (e.g., an individual treated by the method has an increased likelihood of achieving a CR or PR and / or the frequency of CR or PR is increased in the population of individuals treated according to the method). In some aspects, the individual has (i) a Ccr7.2, Cxcr3, Ifit, or Mitotic gene signature score in the sample that is at or above a reference gene signature score or (ii) a Cytotox.2 or Cytotox.4 gene signature score that is below a reference gene signature score and the benefit achieved by the treatment comprising atezolizumab and tiragolumab is an increase in overall survival (OS) hazard ratio (HR) (e.g., an increase in the average OS HR of a population of individuals treated according to the method). In some aspects, the individual has a Ccr7.2, Ccr7.3, or Cxcr3 gene signature score in the sample that is at or above a reference gene signature score and the benefit achieved by the treatment comprising atezolizumab and tiragolumab is an increase in overall survival (OS) (e.g., an increase in the duration of OS experienced by an individual treated according to the method or an increase in the average OS of a population of individuals treated according to the method). An increased clinical response likelihood, OS HR, and / or OS may be determined by comparison to, e.g., an untreated reference individual and / or a reference population of individuals; a reference individual and / or a reference population of individuals who have received a control treatment, such as one or more previously approved treatments or marketed products for treatment of the cancer; and / or a reference individual and / or a reference population of individuals who have been treated with atezolizumab or tiragolumab as a monotherapy. In some aspects, the increased clinical response likelihood, OS HR, and / or OS is determined relative to a reference individual and / or a reference population of individuals having cancer that have been treated with a treatment comprising atezolizumab and tiragolumab, wherein the reference individual and / or each individual in the reference population has (i) a Ccr7.2, Ccr7.3, Cxcr3, Ccl5.1, Ifit, or Mitotic gene signature score that is below a reference gene signature score and / or (ii) a Cytotox.2 or Cytotox.4 gene signature score that is at or above a reference gene signature score. The skilled person is readily able to decide whether a given clinical outcome is improved in accordance with the invention. For example, "improved" in this context means that the clinical outcome resulting from the treatment of an individual having (i) a Ccr7.2, Ccr7.3, Cxcr3, Ccl5.1, Ifit, or Mitotic gene signature score that is at or above a reference gene signature score and / or (ii) a Cytotox.2 or Cytotox.4 gene signature score that is below a reference gene signature score with a treatment comprising atezolizumab and tiragolumab is at least 3% higher, at least 5% higher, at least 7% higher, at least 10% PATENT Attorney Docket No.: 50474-320WO2 Genentech Docket No.: P38318-WO higher, at least 15% higher, at least 20% higher, at least 25% higher, at least 30% higher, at least 40% higher, at least 50% higher, at least 75% higher, at least 100% higher, or at least 120% higher, as compared to the clinical outcome resulting from a comparator treatment as described above. For example, in some aspects, the duration of OS experienced by an individual treated according to the method or the average OS of a population of individuals treated according to the method is increased by at least 3%, at least 5%, at least 7%, at least 10%, at least 15%, at least 20%, at least 25%, at least 30%, at least 40%, at least 50%, at least 75%, at least 100%, or at least 120%. The time at which the clinical outcome / clinical endpoint is assessed can readily be determined by the skilled person. In principle, it is determined at a timepoint when the difference in the clinical outcome / clinical endpoint between the two treatments becomes evident. This time may, for example, be at least 1 month, at least 2 months, at least 3 months, at least 6 months, at least 12 months, at least 18 months, at least 24 months, at least 30 months, at least 36 months, at least 42 months, or at least 48 months after the beginning of the treatment. D. Samples, expression levels, and PD-L1 status Samples An expression level of one or more of CCL5, CXCR3, CCR7, or CXCR6; a member of any one of the Ccr7.2, Ccr7.3, Cxcr3, Ccl5.1, Ifit, Mitotic, Cytotox.2, and Cytotox.4 gene signatures and / or a gene signature score may be determined from any suitable sample. Exemplary sample types include, without limitation, a tissue sample, a tumor sample, a blood sample (e.g., a whole blood sample), a plasma sample, a serum sample, and combinations thereof. Samples may be fresh, archival, or frozen. In some aspects, the sample is a tissue sample, e.g., a tumor tissue sample. In some aspects, the tumor tissue sample is a biopsy, e.g., a biopsy of the NSCLC. In some aspects, the sample is a tumor draining lymph node (dLN) sample. In some aspects, the sample is obtained from the individual prior to treatment with atezolizumab and tiragolumab, e.g., is obtained immediately prior to the first administration of atezolizumab and / or tiragolumab, or is obtained at least one day, at least one week, or at least one month prior to the first administration of atezolizumab and / or tiragolumab. Expression levels The expression levels of the one or more genes detected in the methods provided herein may be, e.g., nucleic acid expression levels or protein expression levels. In some aspects, the expression levels are nucleic acid expression levels, e.g., mRNA expression levels. Nucleic acid expression levels may be detected using any suitable method known in the art, e.g., may be determined by RNA-seq, reverse transcriptase quantitative PCR (RT-qPCR), quantitative PCR (qPCR), real-time PCR, quantitative real-time PCR (qRT-PCR), multiplex qPCR or RT-qPCR, microarray analysis, SAGE, MassARRAY technique, in situ hybridization (ISH), or a combination thereof. Other amplification-based methods include, for example, transcript-mediated amplification (TMA), strand displacement amplification (SDA), nucleic acid sequence based amplification (NASBA), and signal amplification methods such as bDNA. PATENT Attorney Docket No.: 50474-320WO2 Genentech Docket No.: P38318-WO In some instances, nucleic acid expression levels of the genes described herein may be measured by sequencing-based techniques, such as, for example, RNA-seq, serial analysis of gene expression (SAGE), high-throughput sequencing technologies (e.g., massively parallel sequencing), and Sequenom MassARRAY® technology. Nucleic acid expression levels also may be measured by, for example, NanoString nCounter, and high-coverage expression profiling (HiCEP). Additional protocols for evaluating the status of genes and gene products are found, for example in Ausubel et al., eds., 1995, Current Protocols In Molecular Biology, Units 2 (Northern Blotting), 4 (Southern Blotting), 15 (Immunoblotting) and 18 (PCR Analysis). Other methods for detecting nucleic acid levels of the genes described herein include protocols which examine or detect mRNAs, such as target mRNAs, in a tissue or cell sample by microarray technologies. Other methods to detect nucleic acid expression levels of the genes described herein include electrophoresis, Northern and Southern blot analyses, in situ hybridization (e.g., single or multiplex nucleic acid in situ hybridization), RNAse protection assays, and microarrays (e.g., Illumina BEADARRAY™ technology; Beads Array for Detection of Gene Expression (BADGE)). In some aspects, the expression level is a protein expression level, e.g., a protein expression level determined by mass spectrometry, Western blot, ELISA, immunoprecipitation, immunohistochemistry, immunofluorescence, radioimmunoassay, dot blotting, immunodetection methods, surface plasmon resonance, optical spectroscopy, mass spectrometry, or HPLC. Normalization of expression levels In some aspects, the expression levels of one or more genes detected in the methods provided herein are normalized expression levels, e.g., gene signature score is an average of the normalized expression levels of the one or more genes in the sample from the individual. The detected expression level of a gene may be normalized using any one of the standard normalization methods known in the art. One of skill in the art will appreciate that the normalization method used may depend on the gene expression methodology used (e.g., one or more housekeeping genes may be used for normalization in the context of an RT-qPCR methodology, but a whole genome or substantially whole genome may be used as a normalization baseline in the context of an RNA-seq methodology). For example, the detected expression level of each gene assayed can be normalized for differences in the amount of the gene(s) assayed, variability in the quality of the samples used, and / or variability between assay runs. In some instances, normalization may be accomplished by detecting expression of certain one or more normalizing gene(s), including reference gene(s) (e.g., a housekeeping gene (e.g., β-actin)). For example, in some instances, the nucleic acid expression levels detected using the methods described herein may be normalized to the expression level of one or more reference genes (e.g., one, two, three, four, five, six, seven, eight, nine, or more reference genes, e.g., a housekeeping gene (e.g., β-actin)). Alternatively, normalization can be based on the average signal or median signal of all of the assayed genes. On a gene-by-gene basis, a measured normalized amount of an mRNA can be compared to the amount found in a reference expression level. The presence and / or expression level / amount measured PATENT Attorney Docket No.: 50474-320WO2 Genentech Docket No.: P38318-WO in a particular subject sample to be analyzed will fall at some percentile within this range, which can be determined by methods well known in the art. In other instances, to determine an expression level, the detected expression level of each assayed gene is not normalized. Any statistical approaches known in the art may be used to determine the expression level of each gene. For example, the expression level may reflect the median expression level, median normalized expression level, or mean expression level, or mean normalized expression level. Reference expression levels and gene signature scores The terms “reference expression level” and “reference gene signature score” refer to an expression level or a gene signature score against which another expression level or gene signature score is compared, e.g., to make a diagnostic, predictive, prognostic, and / or therapeutic determination. In some aspects, the reference expression level or reference gene signature score is a pre- assigned reference expression level or reference gene signature score. In some aspects, the reference expression level or reference gene signature score is an expression level or a gene signature score in a reference population (e.g., a population of individuals having the NSCLC). In some aspects, the expression level or gene signature score in the reference population is a median expression level or gene signature score of the reference population. In other aspects, the expression level or gene signature score in the reference population is a mean expression level or gene signature score of the reference population. In still other aspects, the expression level or gene signature score is defined as the 25thpercentile, the 26thpercentile, the 27thpercentile, the 28thpercentile, the 29thpercentile, the 30thpercentile, the 31stpercentile, the 32ndpercentile, the 33rdpercentile, the 34thpercentile, the 35thpercentile, the 36thpercentile, the 37thpercentile, the 38thpercentile, the 39thpercentile, the 40thpercentile, the 41stpercentile, the 42ndpercentile, the 43rdpercentile, the 44thpercentile, the 45thpercentile, the 46thpercentile, the 47thpercentile, the 48thpercentile, the 49thpercentile, the 50thpercentile, the 51stpercentile, the 52ndpercentile, the 53rdpercentile, the 54thpercentile, the 55thpercentile, the 56thpercentile, the 57thpercentile, the 58thpercentile, the 59thpercentile, the 60thpercentile, the 61stpercentile, the 62ndpercentile, the 63rdpercentile, the 64thpercentile, the 65thpercentile, the 66thpercentile, the 67thpercentile, the 68thpercentile, the 69thpercentile, the 70thpercentile, the 71stpercentile, the 72ndpercentile, the 73rdpercentile, the 74thpercentile, the 75thpercentile, the 76thpercentile, the 77thpercentile, the 78thpercentile, the 79thpercentile, the 80thpercentile, the 81stpercentile, the 82ndpercentile, the 83rdpercentile, the 84thpercentile, the 85thpercentile, the 86thpercentile, the 87thpercentile, the 88thpercentile, the 89thpercentile, the 90thpercentile, the 91stpercentile, the 92ndpercentile, the 93rdpercentile, the 94thpercentile, the 95thpercentile, the 96thpercentile, the 97thpercentile, the 98thpercentile, or the 99thpercentile of expression levels or TAM signature scores in the reference population. In some instances, the reference expression level or reference gene signature score is a cut-off value that significantly separates a first and a second subset of individuals who have been treated with atezolizumab and tiragolumab in the same reference population based on a significant difference PATENT Attorney Docket No.: 50474-320WO2 Genentech Docket No.: P38318-WO between an individual’s responsiveness to treatment with atezolizumab and tiragolumab above the cut-off value or at or below the cut-off value. In some aspects, the individual’s responsiveness to treatment with atezolizumab and tiragolumab is significantly improved relative to the individual’s responsiveness to treatment with atezolizumab and tiragolumab at or above the cut-off value. In some instances, the reference expression level or reference gene signature score is a cut-off value that significantly separates a first and a second subset of individuals who have been treated with atezolizumab (e.g., atezolizumab monotherapy) in the same reference population based on a significant difference between an individual’s responsiveness to treatment with atezolizumab above the cut-off value or at or below the cut-off value. In some aspects, the individual’s responsiveness to treatment with atezolizumab is significantly improved relative to the individual’s responsiveness to treatment with atezolizumab at or above the cut-off value. PD-L1 status In some aspects, the expression level of PD-L1 has been assessed in the sample from a subject described herein. In some aspects, the sample has been determined to have a PD-L1-positive tumor cell fraction (e.g., by an immunohistochemical (IHC) assay, e.g., by positive staining with an anti-PD-L1 antibody, wherein the anti-PD-L1 antibody is SP263, 22C3, SP142, or 28-8). Exemplary methods for assessing the expression level of PD-L1 are provided in Section II(F). E. Assessment of TIGIT expression In some aspects, the expression of TIGIT is assessed in an individual described herein. The methods provided herein may include determining the expression level of TIGIT in a biological sample (e.g., a tumor sample) obtained from the individual. In other examples, the expression level of TIGIT in a biological sample (e.g., a tumor sample) obtained from the individual has been determined prior to initiation of treatment or after initiation of treatment. TIGIT expression may be determined using any suitable approach. Any suitable tumor sample may be used, e.g., a formalin-fixed and paraffin-embedded (FFPE) tumor sample, an archival tumor sample, a fresh tumor sample, or a frozen tumor sample. For example, TIGIT expression may be determined in terms of the percentage of a tumor sample comprised by tumor-infiltrating immune cells expressing a detectable expression level of TIGIT, as the percentage of tumor-infiltrating immune cells in a tumor sample expressing a detectable expression level of TIGIT, and / or as the percentage of tumor cells in a tumor sample expressing a detectable expression level of TIGIT. It is to be understood that in any of the preceding examples, the percentage of the tumor sample comprised by tumor-infiltrating immune cells may be in terms of the percentage of tumor area covered by tumor-infiltrating immune cells in a section of the tumor sample obtained from the individual, for example, as assessed by IHC using an anti-TIGIT antibody. Any suitable anti-TIGIT antibody may be used. In some examples, the anti-TIGIT antibody is 10A7 (WO 2009 / 126688A3; U.S. Patent No: 9,499,596). In other examples, the anti-TIGIT antibody is the anti-human TIGIT rabbit monoclonal antibody clone SP410 (Roche Tissue Diagnostics, Pleasanton, CA). In some aspects, the anti-TIGIT antibody (e.g., SP410) is detected using the VENTANA OptiView DAB IHC Detection Kit on the automated VENTANA BenchMark ULTRA platform. PATENT Attorney Docket No.: 50474-320WO2 Genentech Docket No.: P38318-WO F. Assessment of PD-L1 expression In some aspects, the expression of PD-L1 is assessed in an individual described herein. The methods provided herein may include determining the expression level of PD-L1 in a biological sample (e.g., a tumor sample) obtained from the individual. In other examples, the expression level of PD-L1 in a biological sample (e.g., a tumor sample) obtained from the individual has been determined prior to initiation of treatment or after initiation of treatment. PD-L1 expression may be determined using any suitable approach. For example, PD-L1 expression may be determined as described in U.S. Patent Application Publication Nos. US20180030138A1 and US20180037655A1. Any suitable tumor sample may be used, e.g., a formalin-fixed and paraffin-embedded (FFPE) tumor sample, an archival tumor sample, a fresh tumor sample, or a frozen tumor sample. For example, PD-L1 expression may be determined in terms of the percentage of a tumor sample comprised by tumor-infiltrating immune cells expressing a detectable expression level of PD-L1, as the percentage of tumor-infiltrating immune cells in a tumor sample expressing a detectable expression level of PD-L1, and / or as the percentage of tumor cells in a tumor sample expressing a detectable expression level of PD-L1. It is to be understood that in any of the preceding examples, the percentage of the tumor sample comprised by tumor-infiltrating immune cells may be in terms of the percentage of tumor area covered by tumor-infiltrating immune cells in a section of the tumor sample obtained from the individual, for example, as assessed by IHC using an anti-PD-L1 antibody (e.g., the SP142 antibody). Any suitable anti-PD-L1 antibody may be used, including, e.g., SP142 (Ventana), SP263 (Ventana), 22C3 (Dako), 28- 8 (Dako), E1L3N (Cell Signaling Technology), 4059 (ProSci, Inc.), h5H1 (Advanced Cell Diagnostics), and 9A11. In some examples, the anti-PD-L1 antibody is SP142. In other examples, the anti-PD-L1 antibody is SP263. In some examples, the anti-PD-L1 antibody is 22C3. In some examples, the anti-PD- L1 antibody is 28-8. In some examples, a tumor sample obtained from the individual has a detectable expression level of PD-L1 in less than 1% of the tumor cells in the tumor sample, in 1% or more of the tumor cells in the tumor sample, in from 1% to less than 5% of the tumor cells in the tumor sample, in 5% or more of the tumor cells in the tumor sample, in from 5% to less than 50% of the tumor cells in the tumor sample, or in 50% or more of the tumor cells in the tumor sample. In some examples, a tumor sample obtained from the individual has a detectable expression level of PD-L1 in tumor-infiltrating immune cells that comprise less than 1% of the tumor sample, more than 1% of the tumor sample, from 1% to less than 5% of the tumor sample, more than 5% of the tumor sample, from 5% to less than 10% of the tumor sample, or more than 10% of the tumor sample. In some aspects, a tumor sample obtained from the individual has a detectable expression level of PD-L1 in tumor-infiltrating immune cells that comprise 5%-19% of the tumor sample (e.g., TIC 5%- 19%); e.g., has a PD-L1 expression level that is PD-L1 low. In some aspects, a tumor sample obtained from the individual has a detectable expression level of PD-L1 in tumor-infiltrating immune cells that comprise ≥20% of the tumor sample (e.g., TIC ≥20%); e.g., has a PD-L1 expression level that is PD-L1 high. In some embodiments, tumor samples that have been determined to have a TIC of greater than, or equal to, 5% are comparable to a CPS of greater than, or equal to, 1. PATENT Attorney Docket No.: 50474-320WO2 Genentech Docket No.: P38318-WO In some examples, tumor samples may be scored for PD-L1 positivity in tumor-infiltrating immune cells and / or in tumor cells according to the criteria for diagnostic assessment shown in Table 1 and / or Table 2, respectively. Table 1. Tumor-infiltrating immune cell (IC) IHC diagnostic criteria Table 2. Tumor cell (TC) IHC diagnostic criteria In some instances, in any of the methods, uses, or compositions for use described herein, the individual has a PD-L1-selected tumor (e.g., a proportion of tumor area occupied by PD-L1 expressing tumor-infiltrating immune cells (ICs) is greater than or equal to 5% in the tumor sample as determined by an IHC with the SP142 antibody). In some instances, the PD-L1-selected tumor is a tumor that has been determined to have a proportion of tumor area occupied by PD-L1 expressing immune cells (ICs) greater than or equal to 5% by an immunohistochemical (IHC) assay. In some instances, the IHC assay uses the anti-PD-L1 antibody SP142, SP263, 22C3, or 28-8. In some instances, the IHC assay uses anti-PD-L1 antibody SP142. In some instances, the IHC assay uses anti-PD-L1 antibody SP263. In some instances, the IHC assay uses anti-PD-L1 antibody 22C3. In some instances, the IHC assay uses anti-PD-L1 antibody 22C3. In some instances, the IHC assay uses anti-PD-L1 antibody 28-8. In some instances, the IC score has been determined to be greater than, or equal to, 5% (e.g., as determined using the Ventana (SP142) PD-L1 IHC assay). In some instances, the IC score has been determined to be 2 or 3 (e.g., as determined using the Ventana (SP142) PD-L1 IHC assay). In some instances, the IC score has been determined to be greater than, or equal to, 1% (e.g., as determined using the Ventana (SP142) PD-L1 IHC assay). In some instances, the IC score has been determined to be greater than, or equal to, 10% (e.g., as determined using the Ventana (SP142) PD-L1 IHC assay). In some instances, the IC score has been determined to be greater than, or equal to, 1% and less than 50% PATENT Attorney Docket No.: 50474-320WO2 Genentech Docket No.: P38318-WO (e.g., as determined using the Ventana (SP142) PD-L1 IHC assay). In some instances, the IC score has been determined to be greater than, or equal to, 1% and less than 30% (e.g., as determined using the Ventana (SP142) PD-L1 IHC assay). In some instances, in any of the methods, uses, or compositions for use described herein, a tumor sample obtained from the individual has a detectable protein expression level of PD-L1. In some instances, the detectable protein expression level of PD-L1 has been determined by an IHC assay. In some instances, the IHC assay uses anti-PD-L1 antibody SP142. In some instances, the tumor sample has been determined to have a detectable expression level of PD-L1 in tumor-infiltrating immune cells that comprise greater than, or equal to, 5% of the tumor sample. In some instances, the tumor sample has been determined to have a detectable expression level of PD-L1 in tumor-infiltrating immune cells that comprise greater than, or equal to, 1% of the tumor sample. In some instances, the tumor sample has been determined to have a detectable expression level of PD-L1 in tumor-infiltrating immune cells that comprise greater than, or equal to, 1% and less than 5% of the tumor sample. In some instances, the tumor sample has been determined to have a detectable expression level of PD-L1 in tumor- infiltrating immune cells that comprise greater than, or equal to, 5% and less than 10% of the tumor sample. In some instances, the tumor sample has been determined to have a detectable expression level of PD-L1 in tumor-infiltrating immune cells that comprise greater than, or equal to, 10% of the tumor sample. In some instances, the tumor sample has been determined to have a detectable expression level of PD-L1 in greater than, or equal to, 1% of the tumor cells in the tumor sample. In some instances, the tumor sample has been determined to have a detectable expression level of PD-L1 in greater than, or equal to, 1% and less than 5% of the tumor cells in the tumor sample. In some instances, the tumor sample has been determined to have a detectable expression level of PD-L1 in greater than, or equal to, 5% and less than 50% of the tumor cells in the tumor sample. In some instances, the tumor sample has been determined to have a detectable expression level of PD-L1 in greater than, or equal to, 50% of the tumor cells in the tumor sample. In some instances, in any of the methods, uses, or compositions for use described herein, the individual has a PD-L1-selected tumor (e.g., a PD-L1 “high”-selected tumor (e.g., a PD-L1 tumor proportion score (TPS) greater than or equal to 50% in a tumor sample as determined by an IHC with the SP263 antibody)). In some instances, the PD-L1-selected tumor is a PD-L1 “high”-selected tumor. In some instances, the PD-L1-selected tumor is a tumor that has been determined to have TPS greater than or equal to 50% by an immunohistochemical (IHC) assay. In some instances, the IHC assay uses the anti-PD-L1 antibody SP263, SP142, 22C3, or 28-8. In some instances, the IHC assay uses anti-PD-L1 antibody SP263. In some instances, the IHC assay uses anti-PD-L1 antibody SP142. In some instances, the IHC assay uses anti-PD-L1 antibody 22C3. In some instances, the TPS has been determined to be greater than, or equal to, 50% (e.g., as determined using the Ventana (SP263) PD-L1 IHC assay). In some instances, the TPS has been determined to be less than 50% (e.g., as determined using the Ventana (SP263) PD-L1 IHC assay). In some instances, the TPS has been determined to be greater than, or equal to, 1% (e.g., as determined using the Ventana (SP263) PD-L1 IHC assay). In some instances, the TPS has been determined to be greater than, or equal to, 1% and less than 50% (e.g., as determined using the Ventana (SP263) PD-L1 IHC assay). PATENT Attorney Docket No.: 50474-320WO2 Genentech Docket No.: P38318-WO In some instances, in any of the methods, uses, or compositions for use described herein, a tumor sample obtained from the individual has a detectable protein expression level of PD-L1. In some instances, the detectable protein expression level of PD-L1 has been determined by an IHC assay. In some instances, the IHC assay uses anti-PD-L1 antibody SP263. In some instances, the tumor sample has been determined to have a PD-L1-positive tumor cell fraction greater than, or equal to, 50% of the tumor sample. In some instances, the tumor sample has been determined to have a PD-L1-positive tumor cell fraction less than 50% of the tumor sample. In some instances, the tumor sample has been determined to have a PD-L1-positive tumor cell fraction greater than, or equal to, 1% and less than 50% of the tumor sample. In some instances, the IHC assay uses the anti-PD-L1 antibody 22C3. In some instances, the IHC assay is the pharmDx 22C3 IHC assay. In some instances, the PD-L1-positive tumor cell fraction is greater than, or equal to, 50% as determined by positive staining with the anti-PD-L1 antibody 22C3. In some embodiments, the tumor sample has been determined to have a combined positive score (CPS) of greater than, or equal to, 10 or a tumor proportion score (TPS) of greater than or equal to 1% in the tumor sample, e.g., as determined using the anti-PD-L1 antibody 22C3 as part of the pharmDx 22C3 IHC assay. In some embodiments, the tumor sample has been determined to have a CPS of greater than, or equal to, 10 or a TPS of greater than or equal to 1% and less than 50% in the tumor sample, e.g., as determined using the anti-PD-L1 antibody 22C3 as part of the pharmDx 22C3 IHC assay. In some embodiments, the tumor sample has been determined to have a CPS of greater than, or equal to, 20 or a TPS of greater than or equal to 50% in the tumor sample, e.g., as determined using the anti-PD-L1 antibody 22C3 as part of the pharmDx 22C3 IHC assay. In some embodiments, tumor samples that have been determined to have a CPS of greater than, or equal to, 1 are comparable to a TIC of greater than, or equal to, 5%. In some instances, the IHC assay uses the anti-PD-L1 antibody 28-8. In some instances, the IHC assay is the pharmDx 28-8 IHC assay. In some instances, the PD-L1-positive tumor cell fraction is greater than, or equal to, 50% as determined by positive staining with the anti-PD-L1 antibody 28-8. In some instances, in any of the methods, uses, or compositions for use described herein, a tumor sample obtained from the individual has a detectable nucleic acid expression level of PD-L1. In some instances, the detectable nucleic acid expression level of PD-L1 has been determined by RNA-seq, RT-qPCR, qPCR, multiplex qPCR or RT-qPCR, microarray analysis, SAGE, MassARRAY technique, ISH, or a combination thereof. In some instances, the sample is selected from the group consisting of a tissue sample, a whole blood sample, a serum sample, and a plasma sample. In some instances, the tissue sample is a tumor sample. In some instances, the tumor sample comprises tumor-infiltrating immune cells, tumor cells, stromal cells, and any combinations thereof. III. TIRAGOLUMAB AND ATEZOLIZUMAB Tiragolumab (an anti-TIGIT antagonist antibody) and atezolizumab (an anti-PD-L1 antibody), which are useful for treating an individual (e.g., a human) having a non-small cell lung cancer (NSCLC) in accordance with the methods, uses, and compositions for use of the invention, are described herein. PATENT Attorney Docket No.: 50474-320WO2 Genentech Docket No.: P38318-WO A. Tiragolumab Tiragolumab (CAS Registry Number: 1918185-84-8) is a fully human IgG1 / kappa MAb that binds TIGIT and comprises the heavy chain sequence of SEQ ID NO: 4 and the light chain sequence of SEQ ID NO: 5. Tiragolumab comprises two N-linked glycosylation sites (N306) in the Fc domain. Tiragolumab is described in WHO Drug Information (International Nonproprietary Names for Pharmaceutical Substances), Proposed INN: List 117, Vol.31, No.2, published June 9, 2017 (see page 343). Tiragolumab (Genentech) is also known as MTIG7192A, RG6058, or RO7092284. Tiragolumab is described in PCT Pub. Nos. WO2003072305A8, WO2004024068A3, WO2004024072A3, WO2009126688A2, WO2015009856A2, WO2016011264A1, WO2016109546A2, WO2017053748A2, and WO2019165434A1; US Pub. Nos.2017 / 0044256, 2017 / 0037127, 2017 / 0145093, 2017 / 260594, 2017 / 0088613, 2018 / 0186875, 2019 / 0119376; and US Pat. Nos. US9873740B2, US10626174B2, US10611836B2, US9499596B2, US8431350B2, US10047158B2, and US10017572B2. B. Atezolizumab Atezolizumab is an anti-PD-L1 antagonist monoclonal antibody (mAb) having the International Nonproprietary Names for Pharmaceutical Substances (INN) List 112 (WHO Drug Information, Vol.28, No.4, 2014, p.488), or the CAS Registry Number 1380723-44-3. C. Methods of delivery The compositions utilized in the methods described herein (e.g., tiragolumab and atezolizumab) can be administered by any suitable method, including, for example, intravenously, intramuscularly, subcutaneously, intradermally, percutaneously, intraarterially, intraperitoneally, intralesionally, intracranially, intraarticularly, intraprostatically, intrapleurally, intratracheally, intrathecally, intranasally, intravaginally, intrarectally, topically, intratumorally, peritoneally, subconjunctivally, intravesicularly, mucosally, intrapericardially, intraumbilically, intraocularly, intraorbitally, orally, topically, transdermally, intravitreally (e.g., by intravitreal injection), by eye drop, by inhalation, by injection, by implantation, by infusion, by continuous infusion, by localized perfusion bathing target cells directly, by catheter, by lavage, in cremes, or in lipid compositions. The compositions utilized in the methods described herein can also be administered systemically or locally. The method of administration can vary depending on various factors (e.g., the compound or composition being administered and the severity of the condition, disease, or disorder being treated). In some aspects, tiragolumab and / or atezolizumab is administered intravenously, intramuscularly, subcutaneously, topically, orally, transdermally, intraperitoneally, intraorbitally, by implantation, by inhalation, intrathecally, intraventricularly, or intranasally. Dosing can be by any suitable route, e.g., by injections, such as intravenous or subcutaneous injections, depending in part on whether the administration is brief or chronic. Various dosing schedules including but not limited to single or multiple administrations over various time-points, bolus administration, and pulse infusion are contemplated herein. Tiragolumab and / or atezolizumab (and any additional therapeutic agent) may be formulated, dosed, and administered in a fashion consistent with good medical practice. Factors for consideration in this context include the particular disorder being treated, the particular mammal being treated, the clinical PATENT Attorney Docket No.: 50474-320WO2 Genentech Docket No.: P38318-WO condition of the individual patient, the cause of the disorder, the site of delivery of the agent, the method of administration, the scheduling of administration, and other factors known to medical practitioners. Tiragolumab and / or atezolizumab need not be, but are optionally formulated with and / or administered concurrently with one or more agents currently used to prevent or treat the disorder in question, e.g., one or more of the agents provided herein. The effective amount of such other agents depends on the amount of tiragolumab or atezolizumab present in the formulation, the type of disorder or treatment, and other factors discussed above. These are generally used in the same dosages and with administration routes as described herein, or about from 1 to 99% of the dosages described herein, or in any dosage and by any route that is empirically / clinically determined to be appropriate. For the treatment of a NSCLC, the appropriate dosage of tiragolumab and atezolizumab, or any combination thereof, described herein (when used alone or in combination with one or more other additional therapeutic agents) will depend on the type of disease to be treated, the severity and course of the disease, whether the tiragolumab and / or atezolizumab is administered for preventive or therapeutic purposes, previous therapy, the patient’s clinical history and response to the tiragolumab and / or atezolizumab, and the discretion of the attending physician. Tiragolumab and / or atezolizumab is suitably administered to the patient at one time or over a series of treatments. One typical daily dosage might range from about 1 μg / kg to 100 mg / kg or more, depending on the factors mentioned above. For repeated administrations over several days or longer, depending on the condition, the treatment would generally be sustained until a desired suppression of disease symptoms occurs. Such doses may be administered intermittently, e.g., every week or every three weeks (e.g., such that the patient receives, for example, from about two to about twenty, or e.g., about six doses of the tiragolumab and / or atezolizumab). An initial higher loading dose, followed by one or more lower doses, may be administered. However, other dosage regimens may be useful. The progress of this therapy is easily monitored by conventional techniques and assays. D. Dosing i. Dosing of tiragolumab As a general proposition, the therapeutically effective amount of tiragolumab administered to a human will be in the range of about 0.01 to about 50 mg / kg of patient body weight, whether by one or more administrations. In some embodiments, the therapeutically effective amount of tiragolumab administered to a human is in the range of 0.01 to 50 mg / kg of patient body weight, whether by one or more administrations. In some exemplary embodiments, tiragolumab is administered in a dose of about 0.01 to about 45 mg / kg, about 0.01 to about 40 mg / kg, about 0.01 to about 35 mg / kg, about 0.01 to about 30 mg / kg, about 0.01 to about 25 mg / kg, about 0.01 to about 20 mg / kg, about 0.01 to about 15 mg / kg, about 0.01 to about 10 mg / kg, about 0.01 to about 5 mg / kg, or about 0.01 to about 1 mg / kg administered daily, weekly, every two weeks, every three weeks, or every four weeks, for example. In exemplary embodiments, tiragolumab is administered in a dose of 0.01 to 45 mg / kg, 0.01 to 40 mg / kg, 0.01 to 35 mg / kg, 0.01 to 30 mg / kg, 0.01 to 25 mg / kg, 0.01 to 20 mg / kg, 0.01 to 15 mg / kg, 0.01 to 10 mg / kg, 0.01 to 5 mg / kg, or 0.01 to 1 mg / kg administered daily, weekly, every two weeks, every three weeks, or every four weeks, for example. PATENT Attorney Docket No.: 50474-320WO2 Genentech Docket No.: P38318-WO In some instances, tiragolumab is administered on about Day 1 (e.g., Day -3, Day -2, Day -1, Day 1, Day 2, or Day 3) of a dosing cycle. In some instances, tiragolumab is administered (e.g., every three weeks) in a tiered dosing regimen (e.g., dosing based on body weight (BW) or body surface area (BSA) of a subject). Such dosing regimens can be utilized in treatments for subjects having relatively low body weight (e.g., 40 kg or less (e.g., from 5 kg to 40 kg, from 15 kg to 40 kg, or from 5 kg to 15 kg)) and have been developed through biosimulation studies based on extrapolations of pharmacokinetic parameters estimated from adult data. In some instances, the effective amount of tiragolumab to treat a subject having a cancer is a tiered dose based on a subject’s body weight. In some instances, the effective amount of tiragolumab is a tiered dose based on a subject’s body weight, wherein the subject has a body weight of (a) less than or equal to 15 kg, and tiragolumab is administered at a dose of between about 10 mg to about 1000 mg every three weeks (e.g., about 300 mg every three weeks); (b) greater than 15 kg and less than or equal to 40 kg, and tiragolumab is administered at a dose of between about 10 mg to about 1000 mg every three weeks (e.g., about 400 mg every three weeks); or (c) greater than 40 kg, and tiragolumab is administered at a dose of between about 30 mg to about 1200 mg every three weeks (e.g., about 600 mg every three weeks). In some instances, the effective amount of tiragolumab is a tiered dose based on a subject’s body weight, wherein the subject has a body weight of (a) less than or equal to 15 kg, and tiragolumab is administered at a dose of between about 250 mg to about 350 mg every three weeks (e.g., about 300 mg every three weeks); (b) greater than 15 kg and less than or equal to 40 kg, and tiragolumab is administered at a dose of between about 350 mg to about 450 mg every three weeks (e.g., about 400 mg every three weeks); or (c) greater than 40 kg, and tiragolumab is administered at a dose of between about 550 mg to about 650 mg every three weeks (e.g., about 600 mg every three weeks). In some instances, the effective amount of tiragolumab is a tiered dose based on a subject’s body weight, wherein the subject has a body weight of (a) less than or equal to 15 kg, and tiragolumab is administered at a dose of about 300 mg every three weeks; (b) greater than 15 kg and less than or equal to 40 kg, and tiragolumab is administered at a dose of about 400 mg every three weeks; or (c) greater than 40 kg, and tiragolumab is administered at a dose of about 600 mg every three weeks. In some instances, the effective amount of tiragolumab is a tiered dose based on a subject’s body weight, wherein the subject has a body weight of (a) less than or equal to 15 kg, and tiragolumab is administered at a dose of between 10 mg to 1000 mg every three weeks (e.g., 300 mg every three weeks); (b) greater than 15 kg and less than or equal to 40 kg, and tiragolumab is administered at a dose of between 10 mg to 1000 mg every three weeks (e.g., 400 mg every three weeks); or (c) greater than 40 kg, and tiragolumab is administered at a dose of between 30 mg to 1200 mg every three weeks (e.g., 600 mg every three weeks). In some instances, the effective amount of tiragolumab is a tiered dose based on a subject’s body weight, wherein the subject has a body weight of (a) less than or equal to 15 kg, and tiragolumab is administered at a dose of between 250 mg to 350 mg every three weeks (e.g., 300 mg every three weeks); (b) greater than 15 kg and less than or equal to 40 kg, and tiragolumab is administered at a dose of between 350 mg to 450 mg every three weeks (e.g., 400 mg every three weeks); or (c) greater than 40 kg, and tiragolumab is administered at a dose of between 550 mg to 650 mg every three weeks (e.g., 600 mg every three weeks). In some instances, the effective amount of tiragolumab is a tiered dose based on PATENT Attorney Docket No.: 50474-320WO2 Genentech Docket No.: P38318-WO a subject’s body weight, wherein the subject has a body weight of (a) less than or equal to 15 kg, and tiragolumab is administered at a dose of 300 mg every three weeks; (b) greater than 15 kg and less than or equal to 40 kg, and tiragolumab is administered at a dose of 400 mg every three weeks; or (c) greater than 40 kg, and tiragolumab is administered at a dose of 600 mg every three weeks. In some instances, the effective amount of tiragolumab is a dose of between about 30 mg to about 1200 mg (e.g., between about 30 mg to about 1100 mg, e.g., between about 60 mg to about 1000 mg, e.g., between about 100 mg to about 900 mg, e.g., between about 200 mg to about 800 mg, e.g., between about 300 mg to about 800 mg, e.g., between about 400 mg to about 800 mg, e.g., between about 400 mg to about 750 mg, e.g., between about 450 mg to about 750 mg, e.g., between about 500 mg to about 700 mg, e.g., between about 550 mg to about 650 mg, e.g., 600 mg ± 10 mg, e.g., 600 ± 6 mg, e.g., 600 ± 5 mg, e.g., 600 ± 3 mg, e.g., 600 ± 1 mg, e.g., 600 ± 0.5 mg, e.g., 600 mg) every three weeks (Q3W) for subject with a body weight greater than 40 kg (e.g., 40.5 kg, 41 kg, 42 kg, 43 kg, 44 kg, 45 kg, 46 kg, 47 kg, 48 kg, 49 kg, 50 kg, 51 kg, 52 kg, 53 kg, 54 kg, 55 kg, 56 kg, 57 kg, 58 kg, 59 kg, 60 kg, 61 kg, 62 kg, 63 kg, 64 kg, 65 kg, 66 kg, 67 kg, 68 kg, 69 kg, 70 kg, 75 kg, 80 kg, 85 kg, 90 kg, 95 kg, 100 kg, 110 kg, 120 kg, 130 kg, 140 kg, 150 kg or more). In some instances, the effective amount of tiragolumab is a dose of about 600 mg every three weeks for subject with a body weight greater than 40 kg. In some instances, the effective amount of tiragolumab is a dose of between 30 mg to 1200 mg (e.g., between 30 mg to 1100 mg, e.g., between 60 mg to 1000 mg, e.g., between 100 mg to 900 mg, e.g., between 200 mg to 800 mg, e.g., between 300 mg to 800 mg, e.g., between 400 mg to 800 mg, e.g., between 400 mg to 750 mg, e.g., between 450 mg to 750 mg, e.g., between 500 mg to 700 mg, e.g., between 550 mg to 650 mg, e.g., 600 mg ± 10 mg, e.g., 600 ± 6 mg, e.g., 600 ± 5 mg, e.g., 600 ± 3 mg, e.g., 600 ± 1 mg, e.g., 600 ± 0.5 mg, e.g., 600 mg) every three weeks (Q3W) for subject with a body weight greater than 40 kg (e.g., 40.5 kg, 41 kg, 42 kg, 43 kg, 44 kg, 45 kg, 46 kg, 47 kg, 48 kg, 49 kg, 50 kg, 51 kg, 52 kg, 53 kg, 54 kg, 55 kg, 56 kg, 57 kg, 58 kg, 59 kg, 60 kg, 61 kg, 62 kg, 63 kg, 64 kg, 65 kg, 66 kg, 67 kg, 68 kg, 69 kg, 70 kg, 75 kg, 80 kg, 85 kg, 90 kg, 95 kg, 100 kg, 110 kg, 120 kg, 130 kg, 140 kg, 150 kg or more). In some instances, the effective amount of tiragolumab is a dose of 600 mg every three weeks for subject with a body weight greater than 40 kg. In some instances, the effective amount of tiragolumab is a dose of between about 10 mg to about 1000 mg (e.g., between about 20 mg to about 1000 mg, e.g., between about 50 mg to about 900 mg, e.g., between about 100 mg to about 850 mg, e.g., between about 200 mg to about 700 mg, e.g., between about 250 mg to about 600 mg, e.g., between about 300 mg to about 500 mg, e.g., between about 350 mg to about 450 mg, e.g., between about 390 mg to about 410 mg, e.g., about 400 mg) every three weeks (Q3W) for subject with a body weight greater than 15 kg and less than or equal to 40 kg (e.g., 15.1 kg, 15.2 kg, 15.3 kg, 15.4 kg, 15.5 kg, 16 kg, 17 kg, 18 kg, 19 kg, 20 kg, 21 kg, 22 kg, 23 kg, 24 kg, 25 kg, 26 kg, 27 kg, 28 kg, 29 kg, 30 kg, 31 kg, 32 kg, 33 kg, 34 kg, 35 kg, 36 kg, 37 kg, 38 kg, 39 kg, or 39.5 kg). In some instances, the effective amount of tiragolumab is a dose of about 400 mg every three weeks (e.g., 400 mg ± 10 mg, e.g., 400 ± 6 mg, e.g., 400 ± 5 mg, e.g., 400 ± 3 mg, e.g., 400 ± 1 mg, e.g., 400 ± 0.5 mg, e.g., 400 mg every three weeks) for subject with a body weight greater than 15 kg and less than or equal to 40 kg. In some instances, the effective amount of tiragolumab is a dose of between 10 mg to 1000 mg (e.g., between 20 mg to 1000 mg, e.g., between 50 mg to 900 mg, e.g., PATENT Attorney Docket No.: 50474-320WO2 Genentech Docket No.: P38318-WO between 100 mg to 850 mg, e.g., between 200 mg to 700 mg, e.g., between 250 mg to 600 mg, e.g., between 300 mg to 500 mg, e.g., between 350 mg to 450 mg, e.g., between 390 mg to 410 mg, e.g., 400 mg) every three weeks (Q3W) for subject with a body weight greater than 15 kg and less than or equal to 40 kg (e.g., 15.1 kg, 15.2 kg, 15.3 kg, 15.4 kg, 15.5 kg, 16 kg, 17 kg, 18 kg, 19 kg, 20 kg, 21 kg, 22 kg, 23 kg, 24 kg, 25 kg, 26 kg, 27 kg, 28 kg, 29 kg, 30 kg, 31 kg, 32 kg, 33 kg, 34 kg, 35 kg, 36 kg, 37 kg, 38 kg, 39 kg, or 39.5 kg). In some instances, the effective amount of tiragolumab is a dose of 400 mg every three weeks (e.g., 400 mg ± 10 mg, e.g., 400 ± 6 mg, e.g., 400 ± 5 mg, e.g., 400 ± 3 mg, e.g., 400 ± 1 mg, e.g., 400 ± 0.5 mg, e.g., 400 mg every three weeks) for subject with a body weight greater than 15 kg and less than or equal to 40 kg. In some instances, the effective amount of tiragolumab is a dose of between about 10 mg to about 1000 mg (e.g., between about 10 mg to about 900 mg, e.g., between about 50 mg to about 900 mg, e.g., between about 100 mg to about 750 mg, e.g., between about 100 mg to about 600 mg, e.g., between about 150 mg to about 500 mg, e.g., between about 200 mg to about 400 mg, e.g., between about 250 mg to about 350 mg, e.g., between about 290 mg to about 310 mg, e.g., about 300 mg) every three weeks (Q3W) for subject with a body weight less than or equal to 15 kg (e.g., 0.5 kg, 1 kg, 1.5 kg, 2.0 kg, 2.5 kg, 3.0 kg, 3.5 kg, 4.0 kg, 4.5 kg, 5.0 kg, 5.5 kg, 6.0 kg, 6.5 kg, 7.0 kg, 7.5 kg, 8.0 kg, 8.5 kg, 9.0 kg, 9.5 kg, 10.0 kg, 10.5 kg, 11.0 kg, 11.5 kg, 12.0 kg, 12.5 kg, 13.0 kg, 13.5 kg, 14.0 kg, 14.5 kg, or 15.0 kg). In some instances, the effective amount of tiragolumab is a dose of about 300 mg every three weeks (e.g., 300 mg ± 10 mg, e.g., 300 ± 6 mg, e.g., 300 ± 5 mg, e.g., 300 ± 3 mg, e.g., 300 ± 1 mg, e.g., 300 ± 0.5 mg, e.g., 300 mg every three weeks) for subject with a body weight less than or equal to 15 kg. In some instances, the effective amount of tiragolumab is a dose of between 10 mg to 1000 mg (e.g., between 10 mg to 900 mg, e.g., between 50 mg to 900 mg, e.g., between 100 mg to 750 mg, e.g., between 100 mg to 600 mg, e.g., between 150 mg to 500 mg, e.g., between 200 mg to 400 mg, e.g., between 250 mg to 350 mg, e.g., between 290 mg to 310 mg, e.g., 300 mg) every three weeks (Q3W) for subject with a body weight less than or equal to 15 kg (e.g., 0.5 kg, 1 kg, 1.5 kg, 2.0 kg, 2.5 kg, 3.0 kg, 3.5 kg, 4.0 kg, 4.5 kg, 5.0 kg, 5.5 kg, 6.0 kg, 6.5 kg, 7.0 kg, 7.5 kg, 8.0 kg, 8.5 kg, 9.0 kg, 9.5 kg, 10.0 kg, 10.5 kg, 11.0 kg, 11.5 kg, 12.0 kg, 12.5 kg, 13.0 kg, 13.5 kg, 14.0 kg, 14.5 kg, or 15.0 kg). In some instances, the effective amount of tiragolumab is a dose of 300 mg every three weeks (e.g., 300 mg ± 10 mg, e.g., 300 ± 6 mg, e.g., 300 ± 5 mg, e.g., 300 ± 3 mg, e.g., 300 ± 1 mg, e.g., 300 ± 0.5 mg, e.g., 300 mg every three weeks) for subject with a body weight less than or equal to 15 kg. In some instances, the effective amount of tiragolumab to treat a subject having a cancer is a tiered dose based on a subject’s body surface area. In some instances, the effective amount of tiragolumab is a tiered dose based on a subject’s body surface area, wherein the subject has a body surface area of (a) less than or equal to 0.5 m2, and tiragolumab is administered at a dose of between about 10 mg to about 1000 mg every three weeks (e.g., about 300 mg every three weeks); (b) greater than 0.5 m2and less than or equal to 0.75 m2, and tiragolumab is administered at a dose of between about 10 mg to about 1000 mg every three weeks (e.g., about 350 mg every three weeks); (c) greater than 0.75 m2and less than or equal to 1.25 m2, and tiragolumab is administered at a dose of between about 10 mg to about 1000 mg every three weeks (e.g., about 450 mg every three weeks); or (d) greater than 1.25 m2, and tiragolumab is administered at a dose of between about 30 mg to about 1200 mg every PATENT Attorney Docket No.: 50474-320WO2 Genentech Docket No.: P38318-WO three weeks (e.g., about 600 mg every three weeks). In some instances, the effective amount of tiragolumab is a tiered dose based on a subject’s body surface area, wherein the subject has a body surface area of (a) less than or equal to 0.5 m2, and tiragolumab is administered at a dose of between about 250 mg to about 350 mg every three weeks (e.g., about 300 mg every three weeks); (b) greater than 0.5 m2and less than or equal to 0.75 m2, and tiragolumab is administered at a dose of between about 300 mg to about 400 mg every three weeks (e.g., about 350 mg every three weeks); or (c) greater than 0.75 m2and less than or equal to 1.25 m2, and tiragolumab is administered at a dose of between about 400 mg to about 500 mg every three weeks (e.g., about 450 mg every three weeks); or (d) greater than 1.25 m2, and tiragolumab is administered at a dose of between about 550 mg to about 650 mg every three weeks (e.g., about 600 mg every three weeks). In some instances, the effective amount of tiragolumab is a tiered dose based on a subject’s body surface area, wherein the subject has a body surface area of (a) less than or equal to 0.5 m2, and tiragolumab is administered at a dose of about 300 mg every three weeks; (b) greater than 0.5 m2and less than or equal to 0.75 m2, and tiragolumab is administered at a dose of about 400 mg every three weeks; (c) greater than 0.75 m2and less than or equal to 1.25 m2, and tiragolumab is administered at a dose of 450 mg every three weeks; or (d) greater than 1.25 m2, and tiragolumab is administered at a dose of about 600 mg every three weeks. In some instances, the effective amount of tiragolumab to treat a subject having a cancer is a tiered dose based on a subject’s body surface area. In some instances, the effective amount of tiragolumab is a tiered dose based on a subject’s body surface area, wherein the subject has a body surface area of (a) less than or equal to 0.5 m2, and tiragolumab is administered at a dose of between 10 mg to 1000 mg every three weeks (e.g., 300 mg every three weeks); (b) greater than 0.5 m2and less than or equal to 0.75 m2, and tiragolumab is administered at a dose of between 10 mg to 1000 mg every three weeks (e.g., 350 mg every three weeks); (c) greater than 0.75 m2and less than or equal to 1.25 m2, and tiragolumab is administered at a dose of between 10 mg to 1000 mg every three weeks (e.g., 450 mg every three weeks); or (d) greater than 1.25 m2, and tiragolumab is administered at a dose of between 30 mg to 1200 mg every three weeks (e.g., 600 mg every three weeks). In some instances, the effective amount of tiragolumab is a tiered dose based on a subject’s body surface area, wherein the subject has a body surface area of (a) less than or equal to 0.5 m2, and tiragolumab is administered at a dose of between 250 mg to 350 mg every three weeks (e.g., 300 mg every three weeks); (b) greater than 0.5 m2and less than or equal to 0.75 m2, and tiragolumab is administered at a dose of between 300 mg to 400 mg every three weeks (e.g., 350 mg every three weeks); or (c) greater than 0.75 m2and less than or equal to 1.25 m2, and tiragolumab is administered at a dose of between 400 mg to 500 mg every three weeks (e.g., 450 mg every three weeks); or (d) greater than 1.25 m2, and tiragolumab is administered at a dose of between 550 mg to 650 mg every three weeks (e.g., 600 mg every three weeks). In some instances, the effective amount of tiragolumab is a tiered dose based on a subject’s body surface area, wherein the subject has a body surface area of (a) less than or equal to 0.5 m2, and tiragolumab is administered at a dose of 300 mg every three weeks; (b) greater than 0.5 m2and less than or equal to 0.75 m2, and tiragolumab is administered at a dose of 400 mg every three weeks; (c) greater than 0.75 m2and less than or equal to 1.25 m2, and tiragolumab is administered at a dose of 450 mg every three weeks; or (d) greater than 1.25 m2, and tiragolumab is administered at a dose of 600 mg every three weeks. PATENT Attorney Docket No.: 50474-320WO2 Genentech Docket No.: P38318-WO In some instances, the effective amount of tiragolumab is a dose of between about 30 mg to about 1200 mg (e.g., between about 30 mg to about 1100 mg, e.g., between about 60 mg to about 1000 mg, e.g., between about 100 mg to about 900 mg, e.g., between about 200 mg to about 800 mg, e.g., between about 300 mg to about 800 mg, e.g., between about 400 mg to about 800 mg, e.g., between about 400 mg to about 750 mg, e.g., between about 450 mg to about 750 mg, e.g., between about 500 mg to about 700 mg, e.g., between about 550 mg to about 650 mg, e.g., 600 mg ± 10 mg, e.g., 600 ± 6 mg, e.g., 600 ± 5 mg, e.g., 600 ± 3 mg, e.g., 600 ± 1 mg, e.g., 600 ± 0.5 mg, e.g., 600 mg) every three weeks (Q3W) for subject with a body surface area greater than 1.25 m2(e.g., 1.25 m2, 1.35 m2, 1.45 m2, 1.50 m2, 1.55 m2, 1.60 m2, 1.65 m2, 1.70 m2, 1.75 m2, 1.80 m2, 1.85 m2, 1.90 m2, 1.95 m2, 2.0 m2, 2.1 m2, 2.2 m2, 2.3 m2, 2.4 m2, 2.5 m2, 2.6 m2, 2.7 m2, 2.8 m2, 2.9 m2, 3.0 m2or more). In some instances, the effective amount of tiragolumab is a dose of about 600 mg every three weeks for subject with a body surface area greater than 1.25 m2. In some instances, the effective amount of tiragolumab is a dose of between 30 mg to 1200 mg (e.g., between 30 mg to 1100 mg, e.g., between 60 mg to 1000 mg, e.g., between 100 mg to 900 mg, e.g., between 200 mg to 800 mg, e.g., between 300 mg to 800 mg, e.g., between 400 mg to 800 mg, e.g., between 400 mg to 750 mg, e.g., between 450 mg to 750 mg, e.g., between 500 mg to 700 mg, e.g., between 550 mg to 650 mg, e.g., 600 mg ± 10 mg, e.g., 600 ± 6 mg, e.g., 600 ± 5 mg, e.g., 600 ± 3 mg, e.g., 600 ± 1 mg, e.g., 600 ± 0.5 mg, e.g., 600 mg) every three weeks (Q3W) for subject with a body surface area greater than 1.25 m2(e.g., 1.25 m2, 1.35 m2, 1.45 m2, 1.50 m2, 1.55 m2, 1.60 m2, 1.65 m2, 1.70 m2, 1.75 m2, 1.80 m2, 1.85 m2, 1.90 m2, 1.95 m2, 2.0 m2, 2.1 m2, 2.2 m2, 2.3 m2, 2.4 m2, 2.5 m2, 2.6 m2, 2.7 m2, 2.8 m2, 2.9 m2, 3.0 m2or more). In some instances, the effective amount of tiragolumab is a dose of 600 mg every three weeks for subject with a body surface area greater than 1.25 m2. In some instances, the effective amount of tiragolumab is a dose of between about 10 mg to about 1000 mg (e.g., between about 20 mg to about 1000 mg, e.g., between about 50 mg to about 900 mg, e.g., between about 100 mg to about 850 mg, e.g., between about 200 mg to about 700 mg, e.g., between about 250 mg to about 600 mg, e.g., between about 300 mg to about 500 mg, e.g., between about 400 mg to about 500 mg, e.g., between about 440 mg to about 460 mg, e.g., about 450 mg) every three weeks (Q3W) for subject with a body surface area greater than 0.75 m2and less than or equal to 1.25 m2(e.g., 0.76 m2, 0.77 m2, 0.78 m2, 0.79 m2, 0.80 m2, 0.82 m2, 0.84 m2, 0.86 m2, 0.88 m2, 0.90 m2, 0.95 m2, 1.0 m2, 1.05 m2, 1.10 m2, 1.15 m2, 1.20 m2, or 1.25 m2). In some instances, the effective amount of tiragolumab is a dose of about 450 mg every three weeks (e.g., 450 mg ± 10 mg, e.g., 450 ± 6 mg, e.g., 450 ± 5 mg, e.g., 450 ± 3 mg, e.g., 450 ± 1 mg, e.g., 450 ± 0.5 mg, e.g., 450 mg every three weeks) for subject with a body surface area greater than 0.75 m2and less than or equal to 1.25 m2. In some instances, the effective amount of tiragolumab is a dose of between about 10 mg to about 1000 mg (e.g., between about 20 mg to about 1000 mg, e.g., between about 50 mg to about 900 mg, e.g., between about 100 mg to about 850 mg, e.g., between about 200 mg to about 700 mg, e.g., between about 250 mg to about 600 mg, e.g., between about 300 mg to about 500 mg, e.g., between about 300 mg to about 400 mg, e.g., between about 340 mg to about 360 mg, e.g., about 350 mg) every three weeks (Q3W) for subject with a body surface area greater than 0.5 m2and less than or equal to 0.75 m2(e.g., 0.51 m2, 0.52 m2, 0.53 m2, 0.54 m2, 0.55 m2, 0.56 m2, 0.57 m2, 0.58 m2, 0.59 m2, 0.60 m2, PATENT Attorney Docket No.: 50474-320WO2 Genentech Docket No.: P38318-WO 0.61 m2, 0.62 m2, 0.63 m2, 0.64 m2, 0.65 m2, 0.66 m2, 0.67 m2, 0.68 m2, 0.69 m2, 0.70 m2, 0.71 m2, 0.72 m2, 0.73 m2, 0.74 m2, or 0.75 m2). In some instances, the effective amount of tiragolumab is a dose of about 350 mg every three weeks (e.g., 350 mg ± 10 mg, e.g., 350 ± 6 mg, e.g., 350 ± 5 mg, e.g., 350 ± 3 mg, e.g., 350 ± 1 mg, e.g., 350 ± 0.5 mg, e.g., 350 mg every three weeks) for subject with a body surface area greater than 0.5 m2and less than or equal to 0.75 m2. In some instances, the effective amount of tiragolumab is a dose of between about 10 mg to about 1000 mg (e.g., between about 10 mg to about 900 mg, e.g., between about 50 mg to about 900 mg, e.g., between about 100 mg to about 750 mg, e.g., between about 100 mg to about 600 mg, e.g., between about 150 mg to about 500 mg, e.g., between about 200 mg to about 400 mg, e.g., between about 250 mg to about 350 mg, e.g., between about 290 mg to about 310 mg, e.g., about 300 mg) every three weeks (Q3W) for subject with a body surface area less than or equal to 0.5 m2(e.g., 0.02 m2, 0.04 m2, 0.06 m2, 0.08 m2, 0.1 m2, 0.15 m2, 0.20 m2, 0.25 m2, 0.30 m2, 0.35 m2, 0.40 m2, 0.45 m2, or 0.50 m2). In some instances, the effective amount of tiragolumab is a dose of about 300 mg every three weeks (e.g., 300 mg ± 10 mg, e.g., 300 ± 6 mg, e.g., 300 ± 5 mg, e.g., 300 ± 3 mg, e.g., 300 ± 1 mg, e.g., 300 ± 0.5 mg, e.g., 300 mg every three weeks) for subject with a body surface area less than or equal to 0.5 m2. In some instances, the effective amount of tiragolumab is a dose (e.g., a fixed dose) of between about 10 mg to about 1000 mg (e.g., between about 20 mg to about 1000 mg, e.g., between about 50 mg to about 900 mg, e.g., between about 100 mg to about 850 mg, e.g., between about 200 mg to about 800 mg, e.g., between about 300 mg to about 600 mg, e.g., between about 400 mg to about 500 mg, e.g., between about 405 mg to about 450 mg, e.g., between about 410 mg to about 430 mg, e.g., about 420 mg) every two weeks (Q2W). In some instances, the effective amount of tiragolumab is a dose of about 420 mg every two weeks (e.g., 420 mg ± 10 mg, e.g., 420 ± 6 mg, e.g., 420 ± 5 mg, e.g., 420 ± 3 mg, e.g., 420 ± 1 mg, e.g., 420 ± 0.5 mg, e.g., 420 mg every two weeks). In some instances, the method comprises administering to the subject or population of subjects tiragolumab at a dose of about 300 mg to about 600 mg every two weeks. In some instances, the method comprises administering to the subject or population of subjects tiragolumab at a dose of 300 mg to 600 mg every two weeks. In some instances, the method comprises administering to the subject or population of subjects tiragolumab at a dose of about 420 every two weeks. In some instances, the method comprises administering to the subject or population of subjects tiragolumab at a dose of 420 every two weeks. In some instances, the dose of tiragolumab is a fixed dose. In some instances, the effective amount of tiragolumab is a dose (e.g., a fixed dose) of between about 30 mg to about 1200 mg (e.g., between about 30 mg to about 1100 mg, e.g., between about 60 mg to about 1000 mg, e.g., between about 100 mg to about 900 mg, e.g., between about 200 mg to about 800 mg, e.g., between about 300 mg to about 800 mg, e.g., between about 400 mg to about 800 mg, e.g., between about 400 mg to about 750 mg, e.g., between about 450 mg to about 750 mg, e.g., between about 500 mg to about 700 mg, e.g., between about 550 mg to about 650 mg, e.g., 600 mg ± 10 mg, e.g., 600 ± 6 mg, e.g., 600 ± 5 mg, e.g., 600 ± 3 mg, e.g., 600 ± 1 mg, e.g., 600 ± 0.5 mg, e.g., 600 mg) every three weeks (Q3W). In some instances, the effective amount of tiragolumab is a dose of about 600 mg every three weeks. In some instances, the method comprises administering to the subject or population of subjects tiragolumab at a dose of about 600 every three weeks. In some instances, the method PATENT Attorney Docket No.: 50474-320WO2 Genentech Docket No.: P38318-WO comprises administering to the subject or population of subjects tiragolumab at a dose of 600 mg every three weeks. In some instances, the dose of tiragolumab is a fixed dose. In some instances, the effective amount of tiragolumab is a dose of between about 200 mg to about 2000 mg (e.g., between about 200 mg to about 2000 mg, e.g., between about 400 mg to about 1900 mg, e.g., between about 500 mg to about 1800 mg, e.g., between about 600 mg to about 1700 mg, e.g., between about 700 mg to about 1400 mg, e.g., between about 800 mg to about 1600 mg, e.g., between about 900 mg to about 1500 mg, e.g., between about 1000 mg to about 1400 mg, e.g., between about 1050 mg to about 1350 mg, e.g., between about 1100 mg to about 1300 mg, e.g., between about 1150 mg to about 1250 mg, e.g., between about 1175 mg to about 1225 mg, e.g., between about 1190 mg to about 1210 mg, e.g., about 1200 mg, e.g., 1200 mg ± 10 mg, e.g., 1200 ± 6 mg, e.g., 1200 ± 5 mg, e.g., 1200 ± 3 mg, e.g., 1200 ± 1 mg, e.g., 1200 ± 0.5 mg, e.g., 1200 mg) every three weeks (Q3W). In some instances, the effective amount of tiragolumab is a dose of about 600 mg every three weeks. In some instances, the effective amount of tiragolumab is a dose of 600 mg every three weeks. In some instances, the effective amount of tiragolumab is a dose of between about 200 mg to about 2000 mg (e.g., between about 200-300 mg, between about 300-400 mg, between about 400-500 mg, between about 500-600 mg, between about 600-700 mg, between about 700-800 mg, between about 800-900 mg, between about 900-1000 mg, between about 1000-1100 mg, between about 1100-1200 mg, between about 1200-1300 mg, between about 1300-1400 mg, between about 1400-1500 mg, between about 1500-1600 mg, between about 1600-1700 mg, between about 1700-1800 mg, between about 1800-1900 mg, or between about 1900-2000 mg, e.g., between about 200 mg to about 1600 mg, e.g., between about 250 mg to about 1600 mg, e.g., between about 300 mg to about 1600 mg, e.g., between about 400 mg to about 1500 mg, e.g., between about 500 mg to about 1400 mg, e.g., between about 600 mg to about 1200 mg, e.g., between about 700 mg to about 1100 mg, e.g., between about 800 mg to about 1000 mg, e.g., between about 800 mg to about 900 mg, e.g., about 200, about 250, about 300, about 350, about 400, about 450, about 500, about 550, about 600, about 650, about 700, about 750, about 800, about 850, about 900, about 950, about 1000, about 1050, about 1100, about 1150, about 1200, about 1250, about 1300, about 1350, about 1400, about 1450, about 1500, about 1550, about 1600 mg, about 1650 mg, about 1700 mg, about 1750 mg, about 1800 mg, about 1850 mg, about 1900 mg, about 1950 mg, or about 2000 mg, e.g., about 800, about 810, about 820, about 830, about 840, about 850, about 860, about 870, about 880, about 890, or about 900 mg) every four weeks (Q4W). In some instances, the effective amount of tiragolumab is about 700 mg to about 1000 mg every four weeks. In some instances, the effective amount of tiragolumab is 700 mg to 1000 mg every four weeks. In some instances, the effective amount of tiragolumab is about 840 mg every four weeks. In some instances, the effective amount of tiragolumab is 840 mg every four weeks. The 840 mg Q4W dosing regimen is supported by results from PK modeling and simulation and exposure-safety analyses. Briefly, the average concentration following the 840 mg Q4W dosing regimen is similar to that of the 600 mg every 3 weeks dosing regimen, which was evaluated in previous studies. The Cmax of the 840 mg Q4W dosing regimen was simulated to be 28% higher at steady state, relative to the Cmax for the 600 mg every 3 weeks dosing regimen, but falls within the range of observed exposure of the highest administered dose in the clinic (1200 mg every 3 weeks). A preliminary analysis of the tiragolumab exposure-safety PATENT Attorney Docket No.: 50474-320WO2 Genentech Docket No.: P38318-WO relationship based on previous observations (tiragolumab doses of 2−1200 mg every 3 weeks administered as monotherapy or in combination with atezolizumab 1200 mg every 3 weeks) suggest that tiragolumab exhibits a flat exposure-safety relationship. In summary, the 840 mg Q4W dosing regimen can provide comparable safety and efficacy as the 600 mg every-3-weeks dosing regimen, given that the predicted exposure is within the range of observed efficacious exposures and tiragolumab exhibits a flat exposure-safety relationship. In some instances, the effective amount of tiragolumab is a dose of between about 200 mg to about 2000 mg (e.g., between about 200 mg to about 2000 mg, e.g., between about 400 mg to about 1900 mg, e.g., between about 500 mg to about 1800 mg, e.g., between about 600 mg to about 1700 mg, e.g., between about 700 mg to about 1400 mg, e.g., between about 800 mg to about 1600 mg, e.g., between about 900 mg to about 1500 mg, e.g., between about 1000 mg to about 1400 mg, e.g., between about 1050 mg to about 1350 mg, e.g., between about 1100 mg to about 1300 mg, e.g., between about 1150 mg to about 1250 mg, e.g., between about 1175 mg to about 1225 mg, e.g., between about 1190 mg to about 1210 mg (e.g., between 200 mg to 2000 mg, e.g., between 400 mg to 1900 mg, e.g., between 500 mg to 1800 mg, e.g., between 600 mg to 1700 mg, e.g., between 700 mg to 1400 mg, e.g., between 800 mg to 1600 mg, e.g., between 900 mg to 1500 mg, e.g., between 1000 mg to 1400 mg, e.g., between 1050 mg to 1350 mg, e.g., between 1100 mg to 1300 mg, e.g., between 1150 mg to 1250 mg, e.g., between 1175 mg to 1225 mg, e.g., between 1190 mg to 1210 mg), e.g., about 1200 mg, e.g., 1200 mg ± 10 mg, e.g., 1200 ± 6 mg, e.g., 1200 ± 5 mg, e.g., 1200 ± 3 mg, e.g., 1200 ± 1 mg, e.g., 1200 ± 0.5 mg, e.g., 1200 mg) every four weeks (Q4W). In some instances, the effective amount of tiragolumab is a dose of about 840 mg every four weeks (e.g., 840 mg ± 10 mg, e.g., 840 ± 6 mg, e.g., 840 ± 5 mg, e.g., 840 ± 3 mg, e.g., 840 ± 1 mg, e.g., 840 ± 0.5 mg, e.g., 840 mg every four weeks). In some instances, the effective amount of tiragolumab is a dose of 840 mg every four weeks. In some instances, the dose of tiragolumab is a fixed dose. In some instances, the effective amount of tiragolumab is a dose of about 1200 mg every four weeks. In some instances, the dose of tiragolumab administered in a combination therapy (e.g., a combination treatment with atezolizumab) may be reduced as compared to a standard dose of tiragolumab administered as a monotherapy. In some instances, tiragolumab is administered intravenously. Alternatively, in some embodiments, tiragolumab is administered subcutaneously. In some instances, tiragolumab is administered to the patient intravenously at a dose of about 420 mg every 2 weeks, about 600 mg every 3 weeks, or about 840 mg of every 4 weeks. In some instances, tiragolumab is administered to the patient intravenously at a dose of 420 mg every 2 weeks, 600 mg every 3 weeks, or 840 mg of every 4 weeks. In some instances, a subject is administered a total of 1 to 20 doses of tiragolumab, e.g., 1, 2, 3, 4, 5, 6, 7, 8, 9, 10, 11, 12, 13, 14, 15, 16, 17, 18, 19, or 20 doses. In some instances, a subject is administered a total of 1 to 50 doses of tiragolumab, e.g., 1 to 50 doses, 1 to 45 doses, 1 to 40 doses, 1 to 35 doses, 1 to 30 doses, 1 to 25 doses, 1 to 20 doses, 1 to 15 doses, 1 to 10 doses, 1 to 5 doses, 2 to 50 doses, 2 to 45 doses, 2 to 40 doses, 2 to 35 doses, 2 to 30 doses, 2 to 25 doses, 2 to 20 doses, 2 to 15 doses, 2 to 10 doses, 2 to 5 doses, 3 to 50 doses, 3 to 45 doses, 3 to 40 doses, 3 to 35 doses, 3 to 30 PATENT Attorney Docket No.: 50474-320WO2 Genentech Docket No.: P38318-WO doses, 3 to 25 doses, 3 to 20 doses, 3 to 15 doses, 3 to 10 doses, 3 to 5 doses, 4 to 50 doses, 4 to 45 doses, 4 to 40 doses, 4 to 35 doses, 4 to 30 doses, 4 to 25 doses, 4 to 20 doses, 4 to 15 doses, 4 to 10 doses, 4 to 5 doses, 5 to 50 doses, 5 to 45 doses, 5 to 40 doses, 5 to 35 doses, 5 to 30 doses, 5 to 25 doses, 5 to 20 doses, 5 to 15 doses, 5 to 10 doses, 10 to 50 doses, 10 to 45 doses, 10 to 40 doses, 10 to 35 doses, 10 to 30 doses, 10 to 25 doses, 10 to 20 doses, 10 to 15 doses, 15 to 50 doses, 15 to 45 doses, 15 to 40 doses, 15 to 35 doses, 15 to 30 doses, 15 to 25 doses, 15 to 20 doses, 20 to 50 doses, 20 to 45 doses, 20 to 40 doses, 20 to 35 doses, 20 to 30 doses, 20 to 25 doses, 25 to 50 doses, 25 to 45 doses, 25 to 40 doses, 25 to 35 doses, 25 to 30 doses, 30 to 50 doses, 30 to 45 doses, 30 to 40 doses, 30 to 35 doses, 35 to 50 doses, 35 to 45 doses, 35 to 40 doses, 40 to 50 doses, 40 to 45 doses, or 45 to 50 doses. In particular instances, the doses may be administered intravenously. ii. Dosing of atezolizumab As a general proposition, the therapeutically effective amount of atezolizumab to a human will be in the range of about 0.01 to about 50 mg / kg of patient body weight, whether by one or more administrations. In some exemplary embodiments, atezolizumab is administered in a dose of about 0.01 to about 45 mg / kg, about 0.01 to about 40 mg / kg, about 0.01 to about 35 mg / kg, about 0.01 to about 30 mg / kg, about 0.01 to about 25 mg / kg, about 0.01 to about 20 mg / kg, about 0.01 to about 15 mg / kg, about 0.01 to about 10 mg / kg, about 0.01 to about 5 mg / kg, or about 0.01 to about 1 mg / kg administered daily, weekly, every two weeks, every three weeks, or every four weeks, for example. In some exemplary embodiments, atezolizumab is administered in a dose of 0.01 to 45 mg / kg, 0.01 to 40 mg / kg, 0.01 to 35 mg / kg, 0.01 to 30 mg / kg, 0.01 to 25 mg / kg, 0.01 to 20 mg / kg, 0.01 to 15 mg / kg, 0.01 to 10 mg / kg, 0.01 to 5 mg / kg, or 0.01 to 1 mg / kg administered daily, weekly, every two weeks, every three weeks, or every four weeks, for example. In some instances, atezolizumab is administered on about Day 1 (e.g., Day -3, Day -2, Day -1, Day 1, Day 2, or Day 3) of a dosing cycle. In some instances, the effective amount of atezolizumab is a dose (e.g., a fixed dose) of between about 20 mg to about 1600 mg (e.g., between about 40 mg to about 1500 mg, e.g., between about 200 mg to about 1400 mg, e.g., between about 300 mg to about 1400 mg, e.g., between about 400 mg to about 1400 mg, e.g., between about 500 mg to about 1300 mg, e.g., between about 600 mg to about 1200 mg, e.g., between about 700 mg to about 1100 mg, e.g., between about 800 mg to about 1000 mg, e.g., between about 800 mg to about 900 mg, e.g., about 800, about 810, about 820, about 830, about 840, about 850, about 860, about 870, about 880, about 890, or about 900 mg) every two weeks (Q2W). In some instances, the effective amount of atezolizumab is a dose (e.g., a fixed dose) of between 20 mg to 1600 mg (e.g., between 40 mg to 1500 mg, e.g., between 200 mg to 1400 mg, e.g., between 300 mg to 1400 mg, e.g., between 400 mg to 1400 mg, e.g., between 500 mg to 1300 mg, e.g., between 600 mg to 1200 mg, e.g., between 700 mg to 1100 mg, e.g., between 800 mg to 1000 mg, e.g., between 800 mg to 900 mg, e.g., 800, 810, 820, 830, 840, 850, 860, 870, 880, 890, or 900 mg) every two weeks (Q2W). In some instances, the effective amount of atezolizumab is a dose of about 840 mg every two weeks (e.g., 840 mg ± 10 mg, e.g., 840 ± 6 mg, e.g., 840 ± 5 mg, e.g., 840 ± 3 mg, e.g., 840 ± 1 mg, e.g., 840 ± 0.5 PATENT Attorney Docket No.: 50474-320WO2 Genentech Docket No.: P38318-WO mg, e.g., 840 mg every two weeks). In some instances, the effective amount of atezolizumab is a dose of about 840 mg every two weeks. In some instances, the effective amount of atezolizumab is a dose of between about 0.01 mg / kg to about 50 mg / kg of the subject’s body weight (e.g., between about 0.01 mg / kg to about 45 mg / kg, e.g., between about 0.1 mg / kg to about 40 mg / kg, e.g., between about 1 mg / kg to about 35 mg / kg, e.g., between about 2.5 mg / kg to about 30 mg / kg, e.g., between about 5 mg / kg to about 25 mg / kg, e.g., between about 5 mg / kg to about 15 mg / kg, e.g., between about 7.5 mg / kg to about 12.5 mg / kg, e.g., about 10 ± 2 mg / kg, about 10 ± 1 mg / kg, about 10 ± 0.5 mg / kg, about 10 ± 0.2 mg / kg, or about 10 ± 0.1 mg / kg, e.g., about 10 mg / kg) every two weeks. In some instances, the effective amount of atezolizumab is a dose of between about 0.01 mg / kg to about 10 mg / kg of the subject’s body weight (e.g., between about 0.1 mg / kg to about 10 mg / kg, e.g., between about 0.5 mg / kg to about 10 mg / kg, e.g., between about 1 mg / kg to about 10 mg / kg, e.g., between about 2.5 mg / kg to about 10 mg / kg, e.g., between about 5 mg / kg to about 10 mg / kg, e.g., between about 7.5 mg / kg to about 10 mg / kg, e.g., between about 8 mg / kg to about 10 mg / kg, e.g., between about 9 mg / kg to about 10 mg / kg, e.g., between about 9.5 mg / kg to about 10 mg / kg, e.g., about 10 ± 1 mg / kg, e.g., about 10 ± 0.5 mg / kg, e.g., about 10 ± 0.2 mg / kg, e.g., about 10 ± 0.1 mg / kg, e.g., about 10 mg / kg) every two weeks. In some instances, the effective amount of atezolizumab is a dose of between 0.01 mg / kg to 50 mg / kg of the subject’s body weight (e.g., between 0.01 mg / kg to 45 mg / kg, e.g., between 0.1 mg / kg to 40 mg / kg, e.g., between 1 mg / kg to 35 mg / kg, e.g., between 2.5 mg / kg to 30 mg / kg, e.g., between 5 mg / kg to 25 mg / kg, e.g., between 5 mg / kg to 15 mg / kg, e.g., between 7.5 mg / kg to 12.5 mg / kg, e.g., 10 ± 2 mg / kg, 10 ± 1 mg / kg, 10 ± 0.5 mg / kg, 10 ± 0.2 mg / kg, or 10 ± 0.1 mg / kg, e.g., 10 mg / kg) every two weeks. In some instances, the effective amount of atezolizumab is a dose of between 0.01 mg / kg to 10 mg / kg of the subject’s body weight (e.g., between 0.1 mg / kg to 10 mg / kg, e.g., between 0.5 mg / kg to 10 mg / kg, e.g., between 1 mg / kg to 10 mg / kg, e.g., between 2.5 mg / kg to 10 mg / kg, e.g., between 5 mg / kg to 10 mg / kg, e.g., between 7.5 mg / kg to 10 mg / kg, e.g., between 8 mg / kg to 10 mg / kg, e.g., between 9 mg / kg to 10 mg / kg, e.g., between 9.5 mg / kg to 10 mg / kg, e.g., 10 ± 1 mg / kg, e.g., 10 ± 0.5 mg / kg, e.g., 10 ± 0.2 mg / kg, e.g., 10 ± 0.1 mg / kg, e.g., 10 mg / kg) every two weeks. In some instances, the effective amount of atezolizumab is a dose of about 10 mg / kg every two weeks. In some instances, the effective amount of atezolizumab is a dose of 10 mg / kg every two weeks. In some instances, the effective amount of atezolizumab to treat a subject having a cancer is a dose of between about 0.01 mg / kg to about 50 mg / kg of the subject’s body weight (e.g., between about 0.01 mg / kg to about 45 mg / kg, e.g., between about 0.1 mg / kg to about 40 mg / kg, e.g., between about 1 mg / kg to about 35 mg / kg, e.g., between about 2.5 mg / kg to about 30 mg / kg, e.g., between about 5 mg / kg to about 25 mg / kg, e.g., between about 10 mg / kg to about 20 mg / kg, e.g., between about 12.5 mg / kg to about 15 mg / kg, e.g., about 15 ± 2 mg / kg, about 15 ± 1 mg / kg, about 15 ± 0.5 mg / kg, about 15 ± 0.2 mg / kg, or about 15 ± 0.1 mg / kg, e.g., about 15 mg / kg) every three weeks. In some instances, the effective amount of atezolizumab is a dose of between about 0.01 mg / kg to about 15 mg / kg of the subject’s body weight (e.g., between about 0.1 mg / kg to about 15 mg / kg, e.g., between about 0.5 mg / kg to about 15 mg / kg, e.g., between about 1 mg / kg to about 15 mg / kg, e.g., between about 2.5 mg / kg to about 15 mg / kg, e.g., between about 5 mg / kg to about 15 mg / kg, e.g., between about 7.5 mg / kg to about PATENT Attorney Docket No.: 50474-320WO2 Genentech Docket No.: P38318-WO 15 mg / kg, e.g., between about 10 mg / kg to about 15 mg / kg, e.g., between about 12.5 mg / kg to about 15 mg / kg, e.g., between about 14 mg / kg to about 15 mg / kg, e.g., about 15 ± 1 mg / kg, e.g., about 15 ± 0.5 mg / kg, e.g., about 15 ± 0.2 mg / kg, e.g., about 15 ± 0.1 mg / kg, e.g., about 15 mg / kg) every three weeks. In some instances, the effective amount of atezolizumab to treat a subject having a cancer is a dose of between 0.01 mg / kg to 50 mg / kg of the subject’s body weight (e.g., between 0.01 mg / kg to 45 mg / kg, e.g., between 0.1 mg / kg to 40 mg / kg, e.g., between 1 mg / kg to 35 mg / kg, e.g., between 2.5 mg / kg to 30 mg / kg, e.g., between 5 mg / kg to 25 mg / kg, e.g., between 10 mg / kg to 20 mg / kg, e.g., between 12.5 mg / kg to 15 mg / kg, e.g., 15 ± 2 mg / kg, 15 ± 1 mg / kg, 15 ± 0.5 mg / kg, 15 ± 0.2 mg / kg, or 15 ± 0.1 mg / kg, e.g., 15 mg / kg) every three weeks. In some instances, the effective amount of atezolizumab is a dose of between 0.01 mg / kg to 15 mg / kg of the subject’s body weight (e.g., between 0.1 mg / kg to 15 mg / kg, e.g., between 0.5 mg / kg to 15 mg / kg, e.g., between 1 mg / kg to 15 mg / kg, e.g., between 2.5 mg / kg to 15 mg / kg, e.g., between 5 mg / kg to 15 mg / kg, e.g., between 7.5 mg / kg to 15 mg / kg, e.g., between 10 mg / kg to 15 mg / kg, e.g., between 12.5 mg / kg to 15 mg / kg, e.g., between 14 mg / kg to 15 mg / kg, e.g., 15 ± 1 mg / kg, e.g., 15 ± 0.5 mg / kg, e.g., 15 ± 0.2 mg / kg, e.g., 15 ± 0.1 mg / kg, e.g., 15 mg / kg) every three weeks. In some instances, the effective amount of atezolizumab is a dose of about 15 mg / kg administered every three weeks. In some instances, the effective amount of atezolizumab is a dose of about 15 mg / kg administered every three weeks with a maximum dose of 1200 mg every three weeks. In some instances, the dose of atezolizumab administered in a combination therapy (e.g., a combination treatment with tiragolumab) may be reduced as compared to a standard dose of atezolizumab administered as a monotherapy. In some embodiments, atezolizumab is administered at a maximum dose of 1200 mg every three weeks. In some instances, the effective amount of atezolizumab is a dose of between about 80 mg to about 2000 mg (e.g., between about 100 mg to about 1600 mg, e.g., between about 200 mg to about 1600 mg, e.g., between about 300 mg to about 1600 mg, e.g., between about 400 mg to about 1600 mg, e.g., between about 500 mg to about 1600 mg, e.g., between about 600 mg to about 1600 mg, e.g., between about 700 mg to about 1600 mg, e.g., between about 800 mg to about 1600 mg, e.g., between about 900 mg to about 1500 mg, e.g., between about 1000 mg to about 1400 mg, e.g., between about 1050 mg to about 1350 mg, e.g., between about 1100 mg to about 1300 mg, e.g., between about 1150 mg to about 1250 mg, e.g., between about 1175 mg to about 1225 mg, e.g., between about 1190 mg to about 1210 mg, e.g., 1200 mg ± 5 mg, e.g., 1200 ± 2.5 mg, e.g., 1200 ± 1.0 mg, e.g., 1200 ± 0.5 mg, e.g., 1200 mg) every three weeks (Q3W). In some instances, the effective amount of atezolizumab is a dose of about 1200 mg every three weeks (e.g., 1200 mg ± 10 mg, e.g., 1200 ± 6 mg, e.g., 1200 ± 5 mg, e.g., 1200 ± 3 mg, e.g., 1200 ± 1 mg, e.g., 1200 ± 0.5 mg, e.g., 1200 mg every three weeks). In some instances, the effective amount of atezolizumab is a dose of 1200 mg every three weeks. In some instances, the effective amount of atezolizumab is a dose of between about 10 mg and about 800 mg (e.g., between about 10 mg and about 800 mg, e.g., between about 20 mg and about 700 mg, e.g., between about 50 mg and about 600 mg, e.g., between about 75 mg and about 500 mg, e.g., between about 100 mg and about 400 mg, e.g., between about 100 mg and about 300 mg, e.g., between about 125 mg and about 275 mg, e.g., between about 150 mg and about 250 mg, e.g., between about 175 mg and about 225 mg, e.g., between about 190 mg and about 210 mg, e.g., about 200 mg ± 10 mg, PATENT Attorney Docket No.: 50474-320WO2 Genentech Docket No.: P38318-WO e.g., 200 mg ± 7.5 mg, e.g., 200 mg ± 5 mg, e.g., 200 ± 2.5 mg, e.g., 200 ± 1.0 mg, e.g., 200 ± 0.5 mg, e.g., 200 mg) every three weeks (Q3W). In some instances, the effective amount of atezolizumab is a dose of about 200 mg every three weeks (e.g., 200 mg ± 10 mg, e.g., 200 ± 6 mg, e.g., 200 ± 5 mg, e.g., 200 ± 3 mg, e.g., 200 ± 1 mg, e.g., 200 ± 0.5 mg, e.g., 200 mg every three weeks). In some instances, the effective amount of atezolizumab is a dose of about 200 mg every three weeks (e.g., 200 mg ± 10 mg, e.g., 200 ± 6 mg, e.g., 200 ± 5 mg, e.g., 200 ± 3 mg, e.g., 200 ± 1 mg, e.g., 200 ± 0.5 mg, e.g., 200 mg every three weeks). In some instances, the effective amount of atezolizumab is a dose of between 10 mg and 800 mg (e.g., between 10 mg and 800 mg, e.g., between 20 mg and 700 mg, e.g., between 50 mg and 600 mg, e.g., between 75 mg and 500 mg, e.g., between 100 mg and 400 mg, e.g., between 100 mg and 300 mg, e.g., between 125 mg and 275 mg, e.g., between 150 mg and 250 mg, e.g., between 175 mg and 225 mg, e.g., between 190 mg and 210 mg, e.g., 200 mg ± 10 mg, e.g., 200 mg ± 7.5 mg, e.g., 200 mg ± 5 mg, e.g., 200 ± 2.5 mg, e.g., 200 ± 1.0 mg, e.g., 200 ± 0.5 mg, e.g., 200 mg) every three weeks (Q3W). In some instances, the effective amount of atezolizumab is a dose of 200 mg every three weeks (e.g., 200 mg ± 10 mg, e.g., 200 ± 6 mg, e.g., 200 ± 5 mg, e.g., 200 ± 3 mg, e.g., 200 ± 1 mg, e.g., 200 ± 0.5 mg, e.g., 200 mg every three weeks). In some instances, the effective amount of atezolizumab is a dose of 200 mg every three weeks (e.g., 200 mg ± 10 mg, e.g., 200 ± 6 mg, e.g., 200 ± 5 mg, e.g., 200 ± 3 mg, e.g., 200 ± 1 mg, e.g., 200 ± 0.5 mg, e.g., 200 mg every three weeks). In some instances, the effective amount of atezolizumab is a dose of about 200 mg every three weeks. In some instances, the effective amount of atezolizumab is a dose of 200 mg every three weeks. In some instances, the effective amount of atezolizumab is a dose of between about 80 mg to about 3000 mg (e.g., between about 80-200 mg, between about 200-400 mg, between about 400-600 mg, between about 600-800 mg, between about 800-1000 mg, between about 1000-1200 mg, between about 1200-1400 mg, between about 1400-1600 mg, between about 1600-1800 mg, between about 1800-2000 mg, between about 2200-2400 mg, between about 2400-2600 mg, between about 2600-2800 mg, or between about 2800-3000 mg, e.g., between about 100 mg and about 3000 mg, e.g., between about 200 mg and about 2900 mg, e.g., between about 500 mg to about 2800 mg, e.g., between about 600 mg to about 2700 mg, e.g., between about 650 mg to about 2600 mg, e.g., between about 700 mg to about 2500 mg, e.g., between about 1000 mg to about 2400 mg, e.g., between about 1100 mg to about 2300 mg, e.g., between about 1200 mg to about 2200 mg, e.g., between about 1300 mg to about 2100 mg, e.g., between about 1400 mg to about 2000 mg, e.g., between about 1500 mg to about 1900 mg, e.g., between about 1600 mg to about 1800 mg, e.g., between about 1620 mg to about 1700 mg, e.g., between about 1640 mg to about 1690 mg, e.g., between about 1660 mg to about 1680 mg, about 1680 mg, e.g., about 80 mg, about 200 mg, about 400 mg, about 600 mg, about 800 mg, about 1000 mg, about 1200 mg, about 1400 mg, about 1600 mg, about 1800 mg, about 2000 mg, about 2200 mg, about 2400 mg, about 2600 mg, about 2800 mg, or about 3000 mg, e.g., about 1600 mg, about 1610 mg, about 1620 mg, about 1630 mg, about 1640 mg, about 1650 mg, about 1660 mg, about 1670 mg, about 1680 mg, about 1690 mg, or about 1700 mg) every four weeks (Q4W). In some instances, the effective amount of atezolizumab is a dose of between 500 mg to 3000 mg (e.g., between 500 mg to 2800 mg, e.g., between 600 mg to 2700 mg, e.g., between 650 mg to 2600 mg, e.g., between 700 mg to 2500 mg, e.g., between 1000 mg to 2400 mg, e.g., between 1100 mg to 2300 mg, e.g., between 1200 mg to 2200 mg, e.g., PATENT Attorney Docket No.: 50474-320WO2 Genentech Docket No.: P38318-WO between 1300 mg to 2100 mg, e.g., between 1400 mg to 2000 mg, e.g., between 1500 mg to 1900 mg, e.g., between 1600 mg to 1800 mg, e.g., between 1620 mg to 1700 mg, e.g., between 1640 mg to 1690 mg, e.g., between 1660 mg to 1680 mg, 1680 mg, e.g., 1600 mg, 1610 mg, 1620 mg, 1630 mg, 1640 mg, 1650 mg, 1660 mg, 1670 mg, 1680 mg, 1690 mg, or 1700 mg) every four weeks (Q4W). In some instances, the effective amount of atezolizumab is a dose of 1680 mg every four weeks (e.g., 1680 mg ± 10 mg, e.g., 1680 ± 6 mg, e.g., 1680 ± 5 mg, e.g., 1680 ± 3 mg, e.g., 1680 ± 1 mg, e.g., 1680 ± 0.5 mg, e.g., 1680 mg every four weeks). In some instances, the effective amount of atezolizumab is a dose of about 1680 mg every four weeks. In some instances, the effective amount of atezolizumab is a dose of 1680 mg every four weeks. In some instances, the effective amount of atezolizumab is a dose of between about 50 mg to about 2000 mg (e.g., between about 50-100 mg, between about 100-250 mg, between about 250-500 mg, between about 500-750 mg, between about 750-1000 mg, between about 1000-1250 mg, between about 1250-1500 mg, between about 1500-1750 mg, or between about 1750-2000 mg, e.g., between about 100 mg to about 1000 mg, between about 120 mg to about 900 mg, between about 150 mg to about 800 mg, between about 200 mg to about 700 mg, between about 250 mg to about 600 mg, between about 300 mg to about 500 mg, or between about 350 mg to about 450 mg, e.g., between about 50 mg to about 100 mg, between about 100 mg to about 200 mg, between about 200 mg to about 300 mg, between about 300 mg to about 400 mg, between about 400 mg to about 500 mg, between about 500 mg to about 600 mg, between about 600 mg to about 700 mg, between about 700 mg to about 800 mg, or between about 800 mg to about 1000 mg, e.g., about 50 mg, about 100 mg, about 250 mg, about 500 mg, about 750 mg, about 1000 mg, about 1250 mg, about 1500 mg, about 1750 mg, or about 2000 mg, e.g., about 300 mg, about 310 mg, about 320 mg, about 330 mg, about 340 mg, about 350 mg, about 360 mg, about 370 mg, about 380 mg, about 390 mg, about 400 mg, about 410 mg, about 420 mg, about 430 mg, about 440 mg, about 450 mg, about 460 mg, about 470 mg, about 480 mg, about 490 mg, or about 500 mg, e.g., 400 mg) every six weeks (Q6W). In some instances, the effective amount of atezolizumab is a dose of between 50 mg to 2000 mg (e.g., between 100 mg to 1000 mg, between 120 mg to 900 mg, between 150 mg to 800 mg, between 200 mg to 700 mg, between 250 mg to 600 mg, between 300 mg to 500 mg, or between 350 mg to 450 mg, e.g., between 50 mg to 100 mg, between 100 mg to 200 mg, between 200 mg to 300 mg, between 300 mg to 400 mg, between 400 mg to 500 mg, between 500 mg to 600 mg, between 600 mg to 700 mg, between 700 mg to 800 mg, or between 800 mg to 1000 mg, e.g., 300 mg, 310 mg, 320 mg, 330 mg, 340 mg, 350 mg, 360 mg, 370 mg, 380 mg, 390 mg, 400 mg, 410 mg, 420 mg, 430 mg, 440 mg, 450 mg, 460 mg, 470 mg, 480 mg, 490 mg, or 500 mg, e.g., 400 mg) every six weeks (Q6W). In some instances, the effective amount of the anti-PD-1 antagonist antibody (e.g., pembrolizumab) is a dose of about 400 mg every six weeks (e.g., 400 mg ± 10 mg, e.g., 400 ± 6 mg, e.g., 400 ± 5 mg, e.g., 400 ± 3 mg, e.g., 400 ± 1 mg, e.g., 400 ± 0.5 mg, e.g., 400 mg every six weeks). In some instances, the dose of atezolizumab is a fixed dose. In some instances, the effective amount of atezolizumab is a dose of (e.g., a fixed dose) about 400 mg every six weeks. In some instances, the effective amount of atezolizumab is a dose (e.g., a fixed dose) of 400 mg every six weeks. In some instances, atezolizumab is administered intravenously. Alternatively, in some embodiments, atezolizumab is administered subcutaneously. In some instances, atezolizumab is PATENT Attorney Docket No.: 50474-320WO2 Genentech Docket No.: P38318-WO administered to the patient intravenously at a dose of about 840 mg every 2 weeks, about 1200 mg every 3 weeks, or about 1680 mg every 4 weeks. In some instances, atezolizumab is administered to the patient intravenously at a dose of 840 mg every 2 weeks, 1200 mg every 3 weeks, or 1680 mg every 4 weeks. In some instances, a subject is administered a total of 1 to 20 doses of atezolizumab, e.g., 1, 2, 3, 4, 5, 6, 7, 8, 9, 10, 11, 12, 13, 14, 15, 16, 17, 18, 19, or 20 doses. In some instances, a subject is administered a total of 1 to 50 doses of atezolizumab, e.g., 1 to 50 doses, 1 to 45 doses, 1 to 40 doses, 1 to 35 doses, 1 to 30 doses, 1 to 25 doses, 1 to 20 doses, 1 to 15 doses, 1 to 10 doses, 1 to 5 doses, 2 to 50 doses, 2 to 45 doses, 2 to 40 doses, 2 to 35 doses, 2 to 30 doses, 2 to 25 doses, 2 to 20 doses, 2 to 15 doses, 2 to 10 doses, 2 to 5 doses, 3 to 50 doses, 3 to 45 doses, 3 to 40 doses, 3 to 35 doses, 3 to 30 doses, 3 to 25 doses, 3 to 20 doses, 3 to 15 doses, 3 to 10 doses, 3 to 5 doses, 4 to 50 doses, 4 to 45 doses, 4 to 40 doses, 4 to 35 doses, 4 to 30 doses, 4 to 25 doses, 4 to 20 doses, 4 to 15 doses, 4 to 10 doses, 4 to 5 doses, 5 to 50 doses, 5 to 45 doses, 5 to 40 doses, 5 to 35 doses, 5 to 30 doses, 5 to 25 doses, 5 to 20 doses, 5 to 15 doses, 5 to 10 doses, 10 to 50 doses, 10 to 45 doses, 10 to 40 doses, 10 to 35 doses, 10 to 30 doses, 10 to 25 doses, 10 to 20 doses, 10 to 15 doses, 15 to 50 doses, 15 to 45 doses, 15 to 40 doses, 15 to 35 doses, 15 to 30 doses, 15 to 25 doses, 15 to 20 doses, 20 to 50 doses, 20 to 45 doses, 20 to 40 doses, 20 to 35 doses, 20 to 30 doses, 20 to 25 doses, 25 to 50 doses, 25 to 45 doses, 25 to 40 doses, 25 to 35 doses, 25 to 30 doses, 30 to 50 doses, 30 to 45 doses, 30 to 40 doses, 30 to 35 doses, 35 to 50 doses, 35 to 45 doses, 35 to 40 doses, 40 to 50 doses, 40 to 45 doses, or 45 to 50 doses. In particular instances, the doses may be administered intravenously. iii. Dosing cycles for tiragolumab and atezolizumab In any of the methods and uses of the invention, tiragolumab and / or atezolizumab may be administered in one or more dosing cycles (e.g., 1, 2, 3, 4, 5, 6, 7, 8, 9, 10, 11, 12, 13, 14, 15, 16, 17, 18, 19, 20, 21, 22, 23, 24, 25, 26, 27, 28, 29, 30, 31, 32, 33, 34, 35, 36, 37, 38, 39, 40, 41, 42, 43, 44, 45, 46, 47, 48, 49, or 50 or more dosing cycles). In some instances, the dosing cycles of tiragolumab and / or atezolizumab continue until there is a loss of clinical benefit (e.g., confirmed disease progression, drug resistance, death, or unacceptable toxicity). In some instances, the length of each dosing cycle is about 7 to 42 days (e.g., 7 days, 8 days, 9 days, 10 days, 11 days, 12 days, 13 days, 14 days, 15 days, 16 days, 17 days, 18 days, 19 days, 20 days, 21 days, 22 days, 23 days, 24 days, 25 days, 26 days, 27 days, 28 days, 29 days, 30 days, 31 days, 32 days, 33 days, 34 days, 35 days, 36 days, 37 days, 38 days, 39 days, 41 days, 42 days). In some instances, the length of each dosing cycle is about 14 days. In some instances, the length of each dosing cycle is about 21 days. In some instances, the length of each dosing cycle is about 28 days. In some instances, the length of each dosing cycle is about 42 days. In some instances, the length of each dosing cycle is about 7 days. In some instances, tiragolumab is administered on about Day 1 (e.g., Day 1 ± 3 days) of each dosing cycle. In some instances, tiragolumab is administered on about Day 15 (e.g., Day 15 ± 3 days) of each dosing cycle. In some instances, tiragolumab is administered on about Day 22 (e.g., Day 22 ± 3 days) of each dosing cycle. In some instances, tiragolumab is administered on about Day 29 (e.g., Day 29 ± 3 days) of each dosing cycle. For example, tiragolumab may be administered intravenously at a dose (e.g., a fixed dose) of about 600 mg PATENT Attorney Docket No.: 50474-320WO2 Genentech Docket No.: P38318-WO on Day 1 of each 21-day cycle (i.e., at a dose of about 600 mg every three weeks). In another example, tiragolumab is administered intravenously at a dose (e.g., a fixed dose) of about 600 mg on Day 1 and Day 15 of each 28-day cycle (i.e., at a dose of about 420 mg every two weeks). For example, tiragolumab may be administered intravenously at a dose (e.g., a fixed dose) of about 600 mg on Day 1, Day 15, and Day 29 of each 42-day cycle (i.e., at a dose of about 420 mg every two weeks). For example, tiragolumab may be administered intravenously at a dose (e.g., a fixed dose) of about 600 mg on Day 1 and Day 22 of each 42-day cycle (i.e., at a dose of about 600 mg every three weeks). In some instances, atezolizumab is administered on about Day 1 (e.g., Day 1 ± 3 days) of each dosing cycle. In some instances, atezolizumab is administered on about Day 15 (e.g., Day 15 ± 3 days) of each dosing cycle. For example, atezolizumab may be administered intravenously at a dose of about 1200 mg on Day 1 of each 21-day cycle (i.e., at a dose of about 1200 mg every three weeks). For example, atezolizumab may be administered intravenously at a dose of about 1200 mg on Day 1 and Day 15 of each 28-day cycle (i.e., at a dose of about 840 mg every two weeks). In some examples, tiragolumab is administered intravenously at a dose (e.g., a fixed dose) of 600 mg on Day 1 of each 21-day cycle (i.e., at a dose of 600 mg every three weeks). In some instances, atezolizumab is administered on Day 1 (e.g., Day 1 ± 3 days) of each dosing cycle. For example, atezolizumab may be administered intravenously at a dose of 1200 mg on Day 1 of each 21-day cycle (i.e., at a dose of 1200 mg every three weeks). In some instances, tiragolumab and atezolizumab are administered on about Day 1 (e.g., Day 1 ± 3 days) of each dosing cycle. In some instances, tiragolumab is administered intravenously at a dose of about 600 mg on Day 1 of each 21-day cycle (i.e., at a dose of about 600 mg every three weeks) and atezolizumab is administered intravenously at a dose of about 1200 mg on Day 1 of each 21-day cycle (i.e., at a dose of about 1200 mg every three weeks). In some instances, tiragolumab is administered intravenously at a dose of 600 mg on Day 1 of each 21-day cycle (i.e., at a dose of 600 mg every three weeks) and atezolizumab is administered intravenously at a dose of 1200 mg on Day 1 of each 21-day cycle (i.e., at a dose of 1200 mg every three weeks). In other instances, tiragolumab is administered intravenously at a dose of about 420 mg on Day 1 of each 14-day cycle (i.e., at a dose of about 420 mg every two weeks) and atezolizumab is administered intravenously at a dose of about 840 mg on Day 1 of each 14-day cycle (i.e., at a dose of about 840 mg every two weeks). In some instances, tiragolumab is administered intravenously at a dose of 420 mg on Day 1 of each 14-day cycle (i.e., at a dose of about 420 mg every two weeks) and atezolizumab is administered intravenously at a dose of 840 mg on Day 1 of each 14-day cycle (i.e., at a dose of 840 mg every two weeks). In other instances, tiragolumab is administered intravenously at a dose of about 840 mg on Day 1 of each 28-day cycle (i.e., at a dose of about 840 mg every four weeks) and atezolizumab is administered intravenously at a dose of about 1680 mg on Day 1 of each 28-day cycle (i.e., at a dose of about 1680 mg every four weeks). In some instances, tiragolumab is administered intravenously at a dose of 840 mg on Day 1 of each 28-day cycle (i.e., at a dose of 840 mg every four weeks) and atezolizumab is administered intravenously at a dose of 1680 mg on Day 1 of each 28-day cycle (i.e., at a dose of 1680 mg every four weeks). PATENT Attorney Docket No.: 50474-320WO2 Genentech Docket No.: P38318-WO In some instances, tiragolumab administered in a combination therapy (e.g., a combination treatment with atezolizumab) may be reduced as compared to a standard dose of tiragolumab administered as a monotherapy. In some instances, the dose of tiragolumab administered in a combination therapy (e.g., a combination treatment with atezolizumab) may be reduced as compared to a standard dose of tiragolumab administered as a monotherapy. In some instances, the dose of atezolizumab administered in a combination therapy (e.g., a combination treatment with tiragolumab) may be reduced as compared to a standard dose of atezolizumab administered as a monotherapy. In some instances, the dose of atezolizumab administered in a combination therapy (e.g., a combination treatment with tiragolumab) may be reduced as compared to a standard dose of atezolizumab administered as a monotherapy. iv. Intravenous infusion and subcutaneous administration of tiragolumab and atezolizumab In some instances, tiragolumab is administered intravenously. Alternatively, in some embodiments, tiragolumab is administered subcutaneously. In some instances, atezolizumab is administered intravenously. Alternatively, in some embodiments, atezolizumab is administered subcutaneously. In some instances, tiragolumab is administered to the subject or population of subjects by intravenous infusion over about 60 ± 15 minutes (e.g., about 45 minutes, about 46 minutes, about 47 minutes, about 48 minutes, about 49 minutes, about 50 minutes, about 51 minutes, about 52 minutes, about 53 minutes, about 54 minutes, about 55 minutes, about 56 minutes, about 57 minutes, about 58 minutes, about 59 minutes, about 60 minutes, about 61 minutes, about 62 minutes, about 63 minutes, about 64 minutes, about 65 minutes, about 66 minutes, about 67 minutes, about 68 minutes, about 69 minutes, about 70 minutes, about 71 minutes, about 72 minutes, about 73 minutes, about 74 minutes, or about 75 minutes). In some instances, tiragolumab is administered to the subject or population of subjects by intravenous infusion over about 60 ± 10 minutes (e.g., about 50 minutes, about 51 minutes, about 52 minutes, about 53 minutes, about 54 minutes, about 55 minutes, about 56 minutes, about 57 minutes, about 58 minutes, about 59 minutes, about 60 minutes, about 61 minutes, about 62 minutes, about 63 minutes, about 64 minutes, about 65 minutes, about 66 minutes, about 67 minutes, about 68 minutes, about 69 minutes, or about 70 minutes). In some instances, atezolizumab is administered to the subject by intravenous infusion over about 60 ± 15 minutes (e.g., about 45 minutes, about 46 minutes, about 47 minutes, about 48 minutes, about 49 minutes, about 50 minutes, about 51 minutes, about 52 minutes, about 53 minutes, about 54 minutes, about 55 minutes, about 56 minutes, about 57 minutes, about 58 minutes, about 59 minutes, about 60 minutes, about 61 minutes, about 62 minutes, about 63 minutes, about 64 minutes, about 65 minutes, about 66 minutes, about 67 minutes, about 68 minutes, about 69 minutes, about 70 minutes, about 71 minutes, about 72 minutes, about 73 minutes, about 74 minutes, or about 75 minutes). In some instances, tiragolumab is administered to the subject by intravenous infusion over about 30 ± 10 minutes (e.g., about 20 minutes, about 21 minutes, about 22 minutes, about 23 minutes, about 24 minutes, about 25 minutes, about 26 minutes, about 27 minutes, about 28 minutes, about 29 minutes, PATENT Attorney Docket No.: 50474-320WO2 Genentech Docket No.: P38318-WO about 30 minutes, about 31 minutes, about 32 minutes, about 33 minutes, about 34 minutes, about 35 minutes, about 36 minutes, about 37 minutes, about 38 minutes, about 39 minutes, or about 40 minutes). In some instances, atezolizumab is administered to the subject by intravenous infusion over about 30 ± 10 minutes (e.g., about 20 minutes, about 21 minutes, about 22 minutes, about 23 minutes, about 24 minutes, about 25 minutes, about 26 minutes, about 27 minutes, about 28 minutes, about 29 minutes, about 30 minutes, about 31 minutes, about 32 minutes, about 33 minutes, about 34 minutes, about 35 minutes, about 36 minutes, about 37 minutes, about 38 minutes, about 39 minutes, or about 40 minutes). v. Administration order and observation periods In some instances in which both tiragolumab and atezolizumab are administered to a subject or population of subjects, the tiragolumab is administered to the subject before the atezolizumab. In some instances, for example, following administration of tiragolumab and before administration of atezolizumab the method includes an intervening first observation period. In some instances, for example, following administration of tiragolumab, atezolizumab is administered to the subject. In some instances, tiragolumab is first administered to the subject and atezolizumab is administered to the subject following administration of tiragolumab. In some instances, the method further includes a second observation period following administration of atezolizumab. In some instances, the method includes both a first observation period following administration of tiragolumab and second observation period following administration of atezolizumab. In some instances, the first and second observation periods are each between about 30 minutes to about 60 minutes in length. In instances in which the first and second observation periods are each about 60 minutes in length, the method may include recording the subject’s vital signs (e.g., pulse rate, respiratory rate, blood pressure, and temperature) at about 30 ± 10 minutes after administration of tiragolumab or atezolizumab during the first or second observation periods. In instances in which the first and second observation periods are each about 30 minutes in length, the method may include recording the subject’s vital signs (e.g., pulse rate, respiratory rate, blood pressure, and temperature) at about 15 ± 10 minutes after administration of tiragolumab or atezolizumab during the first or second observation periods. In some instances, atezolizumab is administered to the subject or population of subjects before tiragolumab. In some instances, for example, following administration of atezolizumab)) and before administration of tiragolumab, the method includes an intervening first observation period. In some instances, the method further includes a second observation period following administration of tiragolumab. In some instances, the method includes both a first observation period following administration of atezolizumab and a second observation period following administration of tiragolumab. In some instances, the first and second observation periods are each between about 30 minutes to about 60 minutes in length. In instances in which the first and second observation periods are each about 60 minutes in length, the method may include recording the subject’s vital signs (e.g., pulse rate, respiratory rate, blood pressure, and temperature) at about 30 ± 10 minutes after administration of atezolizumab or tiragolumab during the first or second observation periods. In instances in which the first and second PATENT Attorney Docket No.: 50474-320WO2 Genentech Docket No.: P38318-WO observation periods are each about 30 minutes in length, the method may include recording the subject’s vital signs (e.g., pulse rate, respiratory rate, blood pressure, and temperature) at about 15 ± 10 minutes after administration of atezolizumab or tiragolumab during the first or second observation periods. vi. Combination dosing of tiragolumab and atezolizumab In some instances, a dose of an effective amount of tiragolumab is administered with a dose of atezolizumab in a combination therapy (e.g., a combination treatment of tiragolumab with atezolizumab), e.g., for treatment of a subject having a NSCLC. In some instances, tiragolumab is administered every two weeks as described in Section III(D)(i) herein and atezolizumab is administered every two weeks as described in Section III(D)(ii) herein. In some instances, tiragolumab is administered every two weeks as described in Section III(D)(i) herein and atezolizumab is administered every three weeks as described in Section III(D)(ii) herein. In some instances, tiragolumab is administered every two weeks as described in Section III(D)(i) herein and atezolizumab is administered every four weeks as described in Section III(D)(ii) herein. In some instances, tiragolumab is administered every two weeks as described in Section III(D)(i) herein and atezolizumab is administered every six weeks as described in Section III(D)(ii) herein. In some instances, tiragolumab is administered every three weeks as described in Section III(D)(i) herein and atezolizumab is administered every two weeks as described in Section III(D)(ii) herein. In some instances, tiragolumab is administered every three weeks as described in Section III(D)(i) herein and atezolizumab is administered every three weeks as described in Section III(D)(ii) herein. In some instances, tiragolumab is administered every three weeks as described in Section III(D)(i) herein and atezolizumab is administered every four weeks as described in Section III(D)(ii) herein. In some instances, tiragolumab is administered every three weeks as described in Section III(D)(i) herein and atezolizumab is administered every six weeks as described in Section III(D)(ii) herein. In some instances, tiragolumab is administered every four weeks as described in Section III(D)(i) herein and atezolizumab is administered every two weeks as described in Section III(D)(ii) herein. In some instances, tiragolumab is administered every four weeks as described in Section III(D)(i) herein and atezolizumab is administered every three weeks as described in Section III(D)(ii). In some instances, tiragolumab is administered every four weeks as described in Section III(D)(i) herein and atezolizumab is administered every four weeks as described in Section III(D)(ii) herein. In some instances, tiragolumab is administered every four weeks as described in Section III(D)(i) herein and atezolizumab is administered every six weeks as described in Section III(D)(ii) herein. In some instances, tiragolumab is administered every two, three, or four weeks as described in Section III(D)(i) herein and atezolizumab is administered every two, three, four, or six weeks as described in Section III(D)(ii) herein. In some instances, the dose of tiragolumab is a dose of about 600 mg every three weeks. In some instances, the dose of tiragolumab is a dose of 600 mg every three weeks. In some instances, tiragolumab is administered (e.g., every three weeks) in a tiered dosing regimen (e.g., dosing based on body weight (BW) or body surface area (BSA) of a subject) and atezolizumab is administered at a dose from about 0.01 mg / kg to about 50 mg / kg (e.g., about 15 mg / kg) up to 1200 mg, e.g., every three weeks. In some instances, tiragolumab is administered (e.g., every three weeks) in a tiered dosing regimen (e.g., dosing based on body weight (BW) or body surface area (BSA) of a subject) and atezolizumab is PATENT Attorney Docket No.: 50474-320WO2 Genentech Docket No.: P38318-WO administered at a dose from 0.01 mg / kg to 50 mg / kg (e.g., 15 mg / kg) up to 1200 mg, e.g., every three weeks. Such dosing regimens can be utilized in treatments for subjects having relatively low body weight (e.g., 40 kg or less (e.g., from 5 kg to 40 kg, from 15 kg to 40 kg, or from 5 kg to 15 kg)) and have been developed through biosimulation studies based on extrapolations of pharmacokinetic parameters estimated from adult data. In some instances, the dose of tiragolumab is a tiered dose based on a subject’s body weight (e.g., body weight (BW) > 40 kg: 600 mg, BW > 15 kg and ≤ 40 kg: 400 mg, and BW ≤ 15 kg: 300 mg). In some instances, the dose of atezolizumab is a dose based on a subject’s body weight (e.g., 15 mg / kg). In some instances, the dose of atezolizumab is a dose based on a subject’s body surface area (e.g., body surface area (BSA) > 1.25 m2: 600 mg, BSA > 0.75 m2and ≤ 1.25 m2: 450 mg, BSA > 0.5 m2and ≤ 0.75 m2: 350 mg, and BSA ≤ 0.5 m2: 300 mg). In some instances, the dose (e.g., about 600 mg) of tiragolumab is administered in combination with a dose of atezolizumab based on a subject’s body weight (e.g., 15 mg / kg) every three weeks. In some instances, the tiered dose (e.g., body weight (BW) > 40 kg: 600 mg, BW > 15 kg and ≤ 40 kg: 400 mg, and BW ≤ 15 kg: 300 mg) of tiragolumab is administered in combination with a dose of atezolizumab based on a subject’s body weight (e.g., 15 mg / kg) every three weeks. In some instances, the tiered dose (e.g., body weight (BW) > 40 kg: 600 mg, BW > 15 kg and ≤ 40 kg: 400 mg, and BW ≤ 15 kg: 300 mg) of tiragolumab is administered in combination with a dose of atezolizumab based on a subject’s body surface area (e.g., BSA > 1.25 m2: 600 mg, BSA > 0.75 m2and ≤ 1.25 m2: 450 mg, BSA > 0.5 m2and ≤ 0.75 m2: 350 mg, and BSA ≤ 0.5 m2: 300 mg) every three weeks. In some embodiments, atezolizumab is administered at a maximum dose of 1200 mg every three weeks. In some instances, the combination therapy is administered with one or more chemotherapeutic agents (e.g., a platinum-based chemotherapeutic agent (e.g., carboplatin or cisplatin) and / or a non-platinum-based chemotherapeutic agent (e.g., an antimetabolite (e.g., pemetrexed or gemcitabine)). In some instances, the effective amount of tiragolumab to treat a subject having a cancer is a tiered dose based on a subject’s body weight, wherein the subject has a body weight of (a) less than or equal to 15 kg, and tiragolumab is administered at a dose of between about 10 mg to about 1000 mg every three weeks (e.g., about 300 mg every three weeks); (b) greater than 15 kg and less than or equal to 40 kg, and tiragolumab is administered at a dose of between about 10 mg to about 1000 mg every three weeks (e.g., about 400 mg every three weeks); or (c) greater than 40 kg, and tiragolumab is administered at a dose of between about 30 mg to about 1200 mg every three weeks (e.g., about 600 mg every three weeks). In some instances, the effective amount of tiragolumab is a tiered dose based on a subject’s body weight, wherein the ...

Claims

PATENT Attorney Docket No.: 50474-320WO2 Genentech Docket No.: P38318-WO What is claimed is: CLAIMS 1. A method of identifying an individual having a non-small cell lung cancer (NSCLC) who may benefit from a treatment comprising atezolizumab and tiragolumab, the method comprising detecting an expression level of one or more of CCL5, CXCR3, CCR7, and CXCR6 in a sample from the individual, wherein an expression level of one or more of CCL5, CXCR3, CCR7, and CXCR6 that is at or above a reference expression level of CCL5, CXCR3, CCR7, or CXCR6 identifies the individual as one who may benefit from a treatment comprising atezolizumab and tiragolumab.

2. A method for selecting a therapy for an individual having a NSCLC, the method comprising detecting an expression level of one or more of CCL5, CXCR3, CCR7, and CXCR6 in a sample from the individual, wherein an expression level of one or more of CCL5, CXCR3, CCR7, and CXCR6 that is at or above a reference expression level of CCL5, CXCR3, CCR7, or CXCR6 identifies the individual as one who may benefit from a treatment comprising atezolizumab and tiragolumab.

3. The method of claim 1 or 2, wherein the individual has an expression level of one or more of CCL5, CXCR3, CCR7, and CXCR6 in the sample that is at or above a reference expression level of CCL5, CXCR3, CCR7, or CXCR6, and the method further comprises administering to the individual an effective amount of atezolizumab and tiragolumab.

4. A method of treating an individual having a NSCLC, the method comprising: (a) detecting an expression level of one or more of CCL5, CXCR3, CCR7, and CXCR6 in a sample from the individual, wherein the expression level of one or more of CCL5, CXCR3, CCR7, and CXCR6 is at or above a reference expression level of CCL5, CXCR3, CCR7, or CXCR6 and thereby identifies the individual as one who may benefit from a treatment comprising atezolizumab and tiragolumab; and (b) administering an effective amount of atezolizumab and tiragolumab to the individual.

5. A method of treating an individual having a NSCLC, the method comprising administering atezolizumab and tiragolumab to the individual, wherein the individual has been determined to have an expression level of one or more of CCL5, CXCR3, CCR7, and CXCR6 that is at or above a reference expression level of CCL5, CXCR3, CCR7, or CXCR6, thereby identifying the individual as one who may benefit from a treatment comprising atezolizumab and tiragolumab.

6. The method of any one of claims 1-5, wherein the benefit is a clinical response.

7. The method of claim 6, wherein the clinical response is a complete response (CR) or a partial response (PR).PATENT Attorney Docket No.: 50474-320WO2 Genentech Docket No.: P38318-WO 8. The method of any one of claims 1-7, wherein the individual has an expression level of one or more of CCL5, CXCR3, and CCR7 in the sample that is at or above a reference expression level of CCL5, CXCR3, or CCR7 and the benefit is an increase in overall survival (OS) hazard ratio (HR).

9. The method of any one of claims 1-7, wherein the individual has an expression level of one or more of CCL5, CXCR3, and CXCR6 in the sample that is at or above a reference expression level of CCL5, CXCR3, or CXCR6 and the benefit is an increase in overall survival (OS).

10. The method of any one of claims 1-9, wherein the reference expression level of CCL5, CXCR3, or CXCR6 is a pre-assigned expression level.

11. The method of any one of claims 1-10, wherein the reference expression level of CCL5, CXCR3, or CXCR6 is an expression level in a reference population.

12. The method of claim 11, wherein the expression level in the reference population is the median expression level of CCL5, CXCR3, or CXCR6 in the reference population.

13. The method of claim 11 or 12, wherein the reference population is a population of individuals having the NSCLC.

14. A method of identifying an individual having a NSCLC who may benefit from a treatment comprising atezolizumab and tiragolumab, the method comprising detecting an expression level of each of CCL5, CXCR3, and CXCR6 in a sample from the individual and determining a gene signature score therefrom, wherein a gene signature score that is at or above a reference gene signature score identifies the individual as one who may benefit from a treatment comprising atezolizumab and tiragolumab.

15. A method for selecting a therapy for an individual having a NSCLC, the method comprising detecting an expression level of each of CCL5, CXCR3, and CXCR6 in a sample from the individual and determining a gene signature score therefrom, wherein a gene signature score that is at or above a reference gene signature score identifies the individual as one who may benefit from a treatment comprising atezolizumab and tiragolumab.

16. The method of claim 14 or 15, wherein the individual has a gene signature score in the sample that is at or above a reference gene signature score, and the method further comprises administering to the individual an effective amount of atezolizumab and tiragolumab.

17. A method of treating an individual having a NSCLC, the method comprising: (a) detecting an expression level of each of CCL5, CXCR3, and CXCR6 in a sample from the individual and determining a gene signature score therefrom, wherein the gene signature score is at orPATENT Attorney Docket No.: 50474-320WO2 Genentech Docket No.: P38318-WO above a reference gene signature score and thereby identifies the individual as one who may benefit from a treatment comprising atezolizumab and tiragolumab; and (b) administering an effective amount of atezolizumab and tiragolumab to the individual.

18. A method of treating an individual having a NSCLC, the method comprising administering atezolizumab and tiragolumab to the individual, wherein the individual has been determined to have a gene signature score that is at or above a reference gene signature score, thereby identifying the individual as one who may benefit from a treatment comprising atezolizumab and tiragolumab, and wherein the gene signature score is based on the expression level of each of CCL5, CXCR3, and CXCR6 detected in a sample from the individual.

19. The method of any one of claims 14-18, wherein the gene signature score is an average of the expression levels of CCL5, CXCR3, and CXCR6 in the sample from the individual.

20. The method of any one of claims 14-17, wherein the method comprises further detecting the expression level of CCR7 in the sample from the individual.

21. The method of claim 20, wherein the gene signature score is an average of the expression levels of CCL5, CXCR3, CXCR6, and CCR7 in the sample from the individual.

22. The method of claim 18, wherein the expression level of CCR7 has been detected in the sample from the individual.

23. The method of claim 22, wherein the gene signature score is an average of the expression levels of CCL5, CXCR3, CXCR6, and CCR7 in the sample from the individual.

24. The method of any one of claims 14-23, wherein the benefit is a clinical response.

25. The method of claim 24, wherein the clinical response is a CR or a PR.

26. The method of any one of claims 14-25, wherein the benefit is an increase in OS HR.

27. The method of any one of claims 14-26, wherein the benefit is an increase in OS.

28. The method of any one of claims 14-27, wherein the reference gene signature score is a pre- assigned gene signature score.

29. The method of any one of claims 14-28, wherein the reference gene signature score is a gene signature score in a reference population.PATENT Attorney Docket No.: 50474-320WO2 Genentech Docket No.: P38318-WO 30. The method of claim 29, wherein the gene signature score in the reference population is the median gene signature score based on the expression level of each of CCL5, CXCR3, and CXCR6 in the reference population.

31. The method of claim 29 or 30, wherein the reference population is a population of individuals having the NSCLC.

32. A method of identifying an individual having a NSCLC who may benefit from a treatment comprising atezolizumab and tiragolumab, the method comprising: (a) detecting an expression level of each of STAT1, LEF1, IRGM, CCR7, SELL, RPS24, RPS27, GBP2, RPS29, RPS3A, RPS20, KLF2, RPLP1, RPL13, DAPL1, SMC6, RFLNB, and RPS4X in a sample from the individual and determining a Ccr7.2 gene signature score therefrom; (b) detecting an expression level of each of DAPL1, CCR7, SMC4, RGCC, MXD4, CD8A, TCF7, ITGAE, RGS10, ZNRF1, CHD3, CD52, DDIT4, LEF1, IZUMO1R, INPP4B, and RFLNB in a sample from the individual and determining a Ccr7.3 gene signature score therefrom; (c) detecting an expression level of each of CXCR6, CKB, GIMAP5, ID2, LTB, FGL2, RAMP1, LYST, ASB2, IL2RB, CXCR3, SERINC3, INPP4B, ANXA1, XCL2, SOCS2, CD82, CD4, and GIMAP7 in a sample from the individual and determining a Cxcr3 gene signature score therefrom; (d) detecting an expression level of each of CCL5, ITGB1, BTG1, GZMK, LTB, IL7R, ZFP36L2, ITGA4, TXNIP, SLAMF6, HCST, ETS1, CXCR3, MS4A4A, DGKA, and YPEL3 in a sample from the individual and determining a Ccl5.1 gene signature score therefrom; (e) detecting an expression level of each of ISG15, IFIT1B, IFIT3, ISG20, IFI27L2, SAMHD1, ZBP1, SLFN5, IRF7, RTP4, USP18, PHF11, LGALS3BP, BST2, GBP2, IFITM3, STAT1, IFI16, and IFIH1 in a sample from the individual and determining an Ifit gene signature score therefrom; (f) detecting an expression level of each of HSP90AB1, PTMA, XCL2, ODC1, TNFRSF9, ITM2A, MYC, YBX3, HSPA5, GPX1, RPS12, TUBA1B, MCM6, TUBB, MCM3, TPI1, MCM5, DUT, and FTL in a sample from the individual and determining a Mitotic gene signature score therefrom; (g) detecting an expression level of each of HMGB2, TOP2A, MKI67, RRM2, PCLAF, TUBB, BIRC5, LMNB1, UBE2C, PTMA, STMN1, HMGN2, TUBA1B, LY6E, and DUT in a sample from the individual and determining a Cytotox.2 gene signature score therefrom; or (h) detecting an expression level of each of S100A6, NRN1, CXCR6, KLRC1, PDCD1, LGALS1, LAG3, ITGB1, ID2, LGALS3, NRGN, CST7, NKG7, S100A10, TNFRSF9, CD52, VIM, and IFITM2 in a sample from the individual and determining a Cytotox.4 gene signature score therefrom; wherein (i) a Ccr7.2, Ccr7.3, Cxcr3, Ccl5.1, Ifit, or Mitotic gene signature score that is at or above a reference gene signature score identifies the individual as one who may benefit from a treatment comprising atezolizumab and tiragolumab, and (ii) a Cytotox.2 or Cytotox.4 gene signature score that is below a reference gene signature score identifies the individual as one who may benefit from a treatment comprising atezolizumab and tiragolumab.PATENT Attorney Docket No.: 50474-320WO2 Genentech Docket No.: P38318-WO 33. A method for selecting a therapy for an individual having a NSCLC, the method comprising: (a) detecting an expression level of each of STAT1, LEF1, IRGM, CCR7, SELL, RPS24, RPS27, GBP2, RPS29, RPS3A, RPS20, KLF2, RPLP1, RPL13, DAPL1, SMC6, RFLNB, and RPS4X in a sample from the individual and determining a Ccr7.2 gene signature score therefrom; (b) detecting an expression level of each of DAPL1, CCR7, SMC4, RGCC, MXD4, CD8A, TCF7, ITGAE, RGS10, ZNRF1, CHD3, CD52, DDIT4, LEF1, IZUMO1R, INPP4B, and RFLNB in a sample from the individual and determining a Ccr7.3 gene signature score therefrom; (c) detecting an expression level of each of CXCR6, CKB, GIMAP5, ID2, LTB, FGL2, RAMP1, LYST, ASB2, IL2RB, CXCR3, SERINC3, INPP4B, ANXA1, XCL2, SOCS2, CD82, CD4, and GIMAP7 in a sample from the individual and determining a Cxcr3 gene signature score therefrom; (d) detecting an expression level of each of CCL5, ITGB1, BTG1, GZMK, LTB, IL7R, ZFP36L2, ITGA4, TXNIP, SLAMF6, HCST, ETS1, CXCR3, MS4A4A, DGKA, and YPEL3 in a sample from the individual and determining a Ccl5.1 gene signature score therefrom; (e) detecting an expression level of each of ISG15, IFIT1B, IFIT3, ISG20, IFI27L2, SAMHD1, ZBP1, SLFN5, IRF7, RTP4, USP18, PHF11, LGALS3BP, BST2, GBP2, IFITM3, STAT1, IFI16, and IFIH1 in a sample from the individual and determining an Ifit gene signature score therefrom; (f) detecting an expression level of each of HSP90AB1, PTMA, XCL2, ODC1, TNFRSF9, ITM2A, MYC, YBX3, HSPA5, GPX1, RPS12, TUBA1B, MCM6, TUBB, MCM3, TPI1, MCM5, DUT, and FTL in a sample from the individual and determining a Mitotic gene signature score therefrom; (g) detecting an expression level of each of HMGB2, TOP2A, MKI67, RRM2, PCLAF, TUBB, BIRC5, LMNB1, UBE2C, PTMA, STMN1, HMGN2, TUBA1B, LY6E, and DUT in a sample from the individual and determining a Cytotox.2 gene signature score therefrom; or (h) detecting an expression level of each of S100A6, NRN1, CXCR6, KLRC1, PDCD1, LGALS1, LAG3, ITGB1, ID2, LGALS3, NRGN, CST7, NKG7, S100A10, TNFRSF9, CD52, VIM, and IFITM2 in a sample from the individual and determining a Cytotox.4 gene signature score therefrom; wherein (i) a Ccr7.2, Ccr7.3, Cxcr3, Ccl5.1, Ifit, or Mitotic gene signature score that is at or above a reference gene signature score identifies the individual as one who may benefit from a treatment comprising atezolizumab and tiragolumab, and (ii) a Cytotox.2 or Cytotox.4 gene signature score that is below a reference gene signature score identifies the individual as one who may benefit from a treatment comprising atezolizumab and tiragolumab.

34. The method of claim 32 or 33, wherein the individual has (i) a Ccr7.2, Ccr7.3, Cxcr3, Ccl5.1, Ifit, or Mitotic gene signature score in the sample that is at or above a reference gene signature score or (ii) a Cytotox.2 or Cytotox.4 gene signature score that is below a reference gene signature score, and the method further comprises administering to the individual an effective amount of atezolizumab and tiragolumab.PATENT Attorney Docket No.: 50474-320WO2 Genentech Docket No.: P38318-WO 35. A method of treating an individual having a NSCLC, the method comprising: (i) (a) detecting an expression level of each of STAT1, LEF1, IRGM, CCR7, SELL, RPS24, RPS27, GBP2, RPS29, RPS3A, RPS20, KLF2, RPLP1, RPL13, DAPL1, SMC6, RFLNB, and RPS4X in a sample from the individual and determining a Ccr7.2 gene signature score therefrom, wherein the gene signature score is at or above a reference gene signature score and thereby identifies the individual as one who may benefit from a treatment comprising atezolizumab and tiragolumab; (b) detecting an expression level of each of DAPL1, CCR7, SMC4, RGCC, MXD4, CD8A, TCF7, ITGAE, RGS10, ZNRF1, CHD3, CD52, DDIT4, LEF1, IZUMO1R, INPP4B, and RFLNB in a sample from the individual and determining a Ccr7.3 gene signature score therefrom, wherein the gene signature score is at or above a reference gene signature score and thereby identifies the individual as one who may benefit from a treatment comprising atezolizumab and tiragolumab; (c) detecting an expression level of each of CXCR6, CKB, GIMAP5, ID2, LTB, FGL2, RAMP1, LYST, ASB2, IL2RB, CXCR3, SERINC3, INPP4B, ANXA1, XCL2, SOCS2, CD82, CD4, and GIMAP7 in a sample from the individual and determining a Cxcr3 gene signature score therefrom, wherein the gene signature score is at or above a reference gene signature score and thereby identifies the individual as one who may benefit from a treatment comprising atezolizumab and tiragolumab; (d) detecting an expression level of each of CCL5, ITGB1, BTG1, GZMK, LTB, IL7R, ZFP36L2, ITGA4, TXNIP, SLAMF6, HCST, ETS1, CXCR3, MS4A4A, DGKA, and YPEL3 in a sample from the individual and determining a Ccl5.1 gene signature score therefrom, wherein the gene signature score is at or above a reference gene signature score and thereby identifies the individual as one who may benefit from a treatment comprising atezolizumab and tiragolumab; (e) detecting an expression level of each of ISG15, IFIT1B, IFIT3, ISG20, IFI27L2, SAMHD1, ZBP1, SLFN5, IRF7, RTP4, USP18, PHF11, LGALS3BP, BST2, GBP2, IFITM3, STAT1, IFI16, and IFIH1 in a sample from the individual and determining an Ifit gene signature score therefrom, wherein the gene signature score is at or above a reference gene signature score and thereby identifies the individual as one who may benefit from a treatment comprising atezolizumab and tiragolumab; (f) detecting an expression level of each of HSP90AB1, PTMA, XCL2, ODC1, TNFRSF9, ITM2A, MYC, YBX3, HSPA5, GPX1, RPS12, TUBA1B, MCM6, TUBB, MCM3, TPI1, MCM5, DUT, and FTL in a sample from the individual and determining a Mitotic gene signature score therefrom, wherein the gene signature score is at or above a reference gene signature score and thereby identifies the individual as one who may benefit from a treatment comprising atezolizumab and tiragolumab; (g) detecting an expression level of each of HMGB2, TOP2A, MKI67, RRM2, PCLAF, TUBB, BIRC5, LMNB1, UBE2C, PTMA, STMN1, HMGN2, TUBA1B, LY6E, and DUT in a sample from the individual and determining a Cytotox.2 gene signature score therefrom, wherein the gene signature score is below a reference gene signature score and thereby identifies the individual as one who may benefit from a treatment comprising atezolizumab and tiragolumab; or (h) detecting an expression level of each of S100A6, NRN1, CXCR6, KLRC1, PDCD1, LGALS1, LAG3, ITGB1, ID2, LGALS3, NRGN, CST7, NKG7, S100A10, TNFRSF9, CD52, VIM, and IFITM2 in a sample from the individual and determining a Cytotox.4 gene signature score therefrom, wherein thePATENT Attorney Docket No.: 50474-320WO2 Genentech Docket No.: P38318-WO gene signature score is below a reference gene signature score and thereby identifies the individual as one who may benefit from a treatment comprising atezolizumab and tiragolumab; and (ii) administering an effective amount of atezolizumab and tiragolumab to the individual.

36. A method of treating an individual having a NSCLC, the method comprising administering atezolizumab and tiragolumab to the individual, wherein the individual has been determined to have: (a) a Ccr7.2 gene signature score based on an expression level of each of STAT1, LEF1, IRGM, CCR7, SELL, RPS24, RPS27, GBP2, RPS29, RPS3A, RPS20, KLF2, RPLP1, RPL13, DAPL1, SMC6, RFLNB, and RPS4X in a sample from the individual that is at or above a reference Ccr7.2 gene signature score; (b) a Ccr7.3 gene signature based on an expression level of each of DAPL1, CCR7, SMC4, RGCC, MXD4, CD8A, TCF7, ITGAE, RGS10, ZNRF1, CHD3, CD52, DDIT4, LEF1, IZUMO1R, INPP4B, and RFLNB in a sample from the individual that is at or above a reference Ccr7.3 gene signature score; (c) a Cxcr3 gene signature score based on an expression level of each of CXCR6, CKB, GIMAP5, ID2, LTB, FGL2, RAMP1, LYST, ASB2, IL2RB, CXCR3, SERINC3, INPP4B, ANXA1, XCL2, SOCS2, CD82, CD4, and GIMAP7 in a sample from the individual that is at or above a reference Cxcr3 gene signature score; (d) a Ccl5.1 gene signature score based on an expression level of each of CCL5, ITGB1, BTG1, GZMK, LTB, IL7R, ZFP36L2, ITGA4, TXNIP, SLAMF6, HCST, ETS1, CXCR3, MS4A4A, DGKA, and YPEL3 in a sample from the individual that is at or above a reference Ccl5.1 gene signature score; (e) an Ifit gene signature score based on an expression level of each of ISG15, IFIT1B, IFIT3, ISG20, IFI27L2, SAMHD1, ZBP1, SLFN5, IRF7, RTP4, USP18, PHF11, LGALS3BP, BST2, GBP2, IFITM3, STAT1, IFI16, and IFIH1 in a sample from the individual that is at or above a reference Ifit gene signature score; (f) a Mitotic gene signature score based on an expression level of each of HSP90AB1, PTMA, XCL2, ODC1, TNFRSF9, ITM2A, MYC, YBX3, HSPA5, GPX1, RPS12, TUBA1B, MCM6, TUBB, MCM3, TPI1, MCM5, DUT, and FTL in a sample from the individual that is at or above a reference Mitotic gene signature score; (g) a Cytotox.2 gene signature score based on an expression level of each of HMGB2, TOP2A, MKI67, RRM2, PCLAF, TUBB, BIRC5, LMNB1, UBE2C, PTMA, STMN1, HMGN2, TUBA1B, LY6E, and DUT in a sample from the individual that is below a reference Cytotox.2 gene signature score; or (h) a Cytotox.4 gene signature score based on an expression level of each of S100A6, NRN1, CXCR6, KLRC1, PDCD1, LGALS1, LAG3, ITGB1, ID2, LGALS3, NRGN, CST7, NKG7, S100A10, TNFRSF9, CD52, VIM, and IFITM2 in a sample from the individual that is below a reference Cytotox.4 gene signature score; thereby identifying the individual as one who may benefit from a treatment comprising atezolizumab and tiragolumab.PATENT Attorney Docket No.: 50474-320WO2 Genentech Docket No.: P38318-WO 37. The method of any one of claims 32-36, wherein the gene signature score is an average of the expression levels of the members of the gene signature in the sample from the individual.

38. The method of any one of claims 32-37, wherein the individual has a Ccr7.3, Cxcr3, or Ccl5.1 gene signature score in the sample that is at or above a reference gene signature score and the benefit is a clinical response.

39. The method of claim 38, wherein the clinical response is a CR or a PR.

40. The method of any one of claims 32-37, wherein the individual has (i) a Ccr7.2, Cxcr3, Ifit, or Mitotic gene signature score in the sample that is at or above a reference gene signature score or (ii) a Cytotox.2 or Cytotox.4 gene signature score that is below a reference gene signature score and the benefit is an increase in OS HR.

41. The method of any one of claims 32-37, wherein the individual has a Ccr7.2, Ccr7.3, or Cxcr3 gene signature score in the sample that is at or above a reference gene signature score and the benefit is an increase in OS.

42. The method of any one of claims 32-41, wherein the reference gene signature score is a pre- assigned gene signature score.

43. The method of any one of claims 32-42, wherein the reference gene signature score is a gene signature score in a reference population.

44. The method of claim 43, wherein the gene signature score in the reference population is the median Ccr7.2, Ccr7.3, Cxcr3, Ccl5.1, Ifit, Mitotic, Cytotox.2, or Cytotox.4 gene signature score in the reference population.

45. The method of claim 43 or 44, wherein the reference population is a population of individuals having the NSCLC.

46. A method of identifying an individual having a NSCLC who may benefit from a treatment comprising atezolizumab, the method comprising detecting an expression level of each of CCL5, CXCR3, and CXCR6 in a sample from the individual and determining a gene signature score therefrom, wherein a gene signature score that is at or above a reference gene signature score identifies the individual as one who may benefit from a treatment comprising atezolizumab.PATENT Attorney Docket No.: 50474-320WO2 Genentech Docket No.: P38318-WO 47. A method for selecting a therapy for an individual having a NSCLC, the method comprising detecting an expression level of each of CCL5, CXCR3, and CXCR6 in a sample from the individual and determining a gene signature score therefrom, wherein a gene signature score that is at or above a reference gene signature score identifies the individual as one who may benefit from a treatment comprising atezolizumab.

48. The method of claim 46 or 47, wherein the individual has a gene signature score in the sample that is at or above a reference gene signature score, and the method further comprises administering to the individual an effective amount of atezolizumab.

49. A method of treating an individual having a NSCLC, the method comprising: (a) detecting an expression level of each of CCL5, CXCR3, and CXCR6 in a sample from the individual and determining a gene signature score therefrom, wherein the gene signature score is at or above a reference gene signature score and thereby identifies the individual as one who may benefit from a treatment comprising atezolizumab; and (b) administering an effective amount of atezolizumab to the individual.

50. A method of treating an individual having a NSCLC, the method comprising administering atezolizumab to the individual, wherein the individual has been determined to have a gene signature score that is at or above a reference gene signature score, thereby identifying the individual as one who may benefit from a treatment comprising atezolizumab, and wherein the gene signature score is based on the expression level of each of CCL5, CXCR3, and CXCR6 detected in a sample from the individual.

51. The method of any one of claims 46-50, wherein the gene signature score is an average of the expression levels of CCL5, CXCR3, and CXCR6 in the sample from the individual.

52. The method of any one of claims 46-49, wherein the method comprises further detecting the expression level of CCR7 in the sample from the individual.

53. The method of claim 52, wherein the gene signature score is an average of the expression levels of CCL5, CXCR3, CXCR6, and CCR7 in the sample from the individual.

54. The method of claim 50, wherein the expression level of CCR7 has been detected in the sample from the individual.

55. The method of claim 54, wherein the gene signature score is an average of the expression levels of CCL5, CXCR3, CXCR6, and CCR7 in the sample from the individual.

56. The method of any one of claims 46-55, wherein the benefit is an increase in progression-free survival (PFS) or OS.PATENT Attorney Docket No.: 50474-320WO2 Genentech Docket No.: P38318-WO 57. The method of any one of claims 46-56, wherein the reference gene signature score is a pre- assigned gene signature score.

58. The method of any one of claims 46-57, wherein the reference gene signature score is a gene signature score in a reference population.

59. The method of claim 58, wherein the gene signature score in the reference population is the median gene signature score based on the expression level of each of CCL5, CXCR3, and CXCR6 in the reference population.

60. The method of claim 58 or 59, wherein the reference population is a population of individuals having the NSCLC.

61. The method of any one of claims 46-60, wherein the treatment comprising atezolizumab is atezolizumab monotherapy.

62. The method of any one of claims 1-61, wherein the expression level is a nucleic acid expression level or a protein expression level.

63. The method of claim 62, wherein the expression level is a nucleic acid expression level.

64. The method of claim 63, wherein the nucleic acid expression level is determined by RNA-seq, RT-qPCR, qPCR, multiplex qPCR or RT-qPCR, microarray analysis, SAGE, MassARRAY technique, ISH, or a combination thereof.

65. The method of claim 63 or 64, wherein the nucleic acid expression level is an mRNA expression level.

66. The method of claim 65, wherein the mRNA expression level is determined by RNA-seq.

67. The method of claim 62, wherein the expression level is a protein expression level.

68. The method of claim 67, wherein the protein expression level is determined by mass spectrometry.

69. The method of any one of claims 1-68, wherein the sample is obtained from the individual prior to treatment with atezolizumab and / or tiragolumab.PATENT Attorney Docket No.: 50474-320WO2 Genentech Docket No.: P38318-WO 70. The method of any one of claims 1-69, wherein the sample is a tissue sample, a tumor sample, a blood sample, a plasma sample, a serum sample, or a combination thereof.

71. The method of claim 70, wherein the sample is a tissue sample.

72. The method of claim 71, wherein the tissue sample is a tumor tissue sample.

73. The method of claim 72, wherein the tumor tissue sample is a biopsy.

74. The method of claim 71, wherein the tissue sample is a tumor draining lymph node (dLN) sample.

75. The method of claim 70, wherein the sample is a blood sample.

76. The method of any one of claims 70-75, wherein the sample is an archival sample, a fresh sample, or a frozen sample.

77. The method of any one of claims 1-76, wherein the individual has a PD-L1-positive NSCLC.

78. The method of claim 77, wherein the PD-L1-positive NSCLC has been determined to have a PD- L1-positive tumor cell fraction by an immunohistochemical (IHC) assay.

79. The method of claim 78, wherein the PD-L1-positive tumor cell fraction is determined by positive staining with an anti-PD-L1 antibody, wherein the anti-PD-L1 antibody is SP263, 22C3, SP142, or 28-8.

80. The method of any one of claims 1-79, wherein the individual is a human.

81. The method of any one of claims 1-80, wherein the individual has not previously been treated for NSCLC.

82. Use of atezolizumab and / or tiragolumab in the manufacture of a medicament for the treatment of an individual having a NSCLC, wherein the individual has been determined to have an expression level of one or more of CCL5, CXCR3, CCR7, and CXCR6 in a sample from the individual that is at or above a reference expression level of CCL5, CXCR3, CCR7, or CXCR6, thereby identifying the individual as one who may benefit from a treatment comprising atezolizumab and tiragolumab.

83. The use of claim 82, wherein the benefit is a clinical response.

84. The use of claim 83, wherein the clinical response is a complete response (CR) or a partial response (PR).PATENT Attorney Docket No.: 50474-320WO2 Genentech Docket No.: P38318-WO 85. The use of any one of claims 82-84, wherein the individual has been determined to have an expression level of one or more of CCL5, CXCR3, and CCR7 in the sample that is at or above a reference expression level of CCL5, CXCR3, or CCR7 and the benefit is an increase in overall survival (OS) hazard ratio (HR).

86. The use of any one of claims 82-85, wherein the individual has been determined to have an expression level of one or more of CCL5, CXCR3, and CXCR6 in the sample that is at or above a reference expression level of CCL5, CXCR3, or CXCR6 and the benefit is an increase in overall survival (OS).

87. The use of any one of claims 82-86, wherein the reference expression level of CCL5, CXCR3, or CXCR6 is a pre-assigned expression level.

88. The use of any one of claims 82-87, wherein the reference expression level of CCL5, CXCR3, or CXCR6 is an expression level in a reference population.

89. The use of claim 88, wherein the expression level in the reference population is the median expression level of CCL5, CXCR3, or CXCR6 in the reference population.

90. The use of claim 88 or 89, wherein the reference population is a population of individuals having the NSCLC.

91. Use of atezolizumab and / or tiragolumab in the manufacture of a medicament for the treatment of an individual having a NSCLC, wherein the individual has been determined to have a gene signature score that is at or above a reference gene signature score, thereby identifying the individual as one who may benefit from a treatment comprising atezolizumab and tiragolumab, wherein the gene signature score is based on the expression level of each of CCL5, CXCR3, and CXCR6 detected in a sample from the individual.

92. The use of claim 91, wherein the gene signature score is an average of the expression levels of CCL5, CXCR3, and CXCR6 in the sample from the individual.

93. The use of claim 91 or 92, wherein the expression level of CCR7 has been detected in the sample from the individual.

94. The use of claim 93, wherein the gene signature score is an average of the expression levels of CCL5, CXCR3, CXCR6, and CCR7 in the sample from the individual.

95. The use of any one of claims 91-94, wherein the benefit is a clinical response.PATENT Attorney Docket No.: 50474-320WO2 Genentech Docket No.: P38318-WO 96. The use of claim 95, wherein the clinical response is a CR or a PR.

97. The use of any one of claims 91-96, wherein the benefit is an increase in OS HR.

98. The use of any one of claims 91-97, wherein the benefit is an increase in OS.

99. The use of any one of claims 91-98, wherein the reference gene signature score is a pre- assigned gene signature score.

100. The use of any one of claims 91-99, wherein the reference gene signature score is a gene signature score in a reference population.

101. The use of claim 100, wherein the gene signature score in the reference population is the median gene signature score based on the expression level of each of CCL5, CXCR3, and CXCR6 in the reference population.

102. The use of claim 100 or 101, wherein the reference population is a population of individuals having the NSCLC.

103. Use of atezolizumab and / or tiragolumab in the manufacture of a medicament for the treatment of an individual having a NSCLC, wherein the individual has been determined to have: (i) (a) a Ccr7.2 gene signature score that is at or above a reference gene signature score, thereby identifying the individual as one who may benefit from a treatment comprising atezolizumab and tiragolumab, wherein the gene signature score is based on the expression level of each of STAT1, LEF1, IRGM, CCR7, SELL, RPS24, RPS27, GBP2, RPS29, RPS3A, RPS20, KLF2, RPLP1, RPL13, DAPL1, SMC6, RFLNB, and RPS4X detected in a sample from the individual; (b) a Ccr7.3 gene signature score that is at or above a reference gene signature score, thereby identifying the individual as one who may benefit from a treatment comprising atezolizumab and tiragolumab, wherein the gene signature score is based on the expression level of each of DAPL1, CCR7, SMC4, RGCC, MXD4, CD8A, TCF7, ITGAE, RGS10, ZNRF1, CHD3, CD52, DDIT4, LEF1, IZUMO1R, INPP4B, and RFLNB detected in a sample from the individual; (c) a Cxcr3 gene signature score that is at or above a reference gene signature score, thereby identifying the individual as one who may benefit from a treatment comprising atezolizumab and tiragolumab, wherein the gene signature score is based on the expression level of each of CXCR6, CKB, GIMAP5, ID2, LTB, FGL2, RAMP1, LYST, ASB2, IL2RB, CXCR3, SERINC3, INPP4B, ANXA1, XCL2, SOCS2, CD82, CD4, and GIMAP7 detected in a sample from the individual; (d) a Ccl5.1 gene signature score that is at or above a reference gene signature score, thereby identifying the individual as one who may benefit from a treatment comprising atezolizumab andPATENT Attorney Docket No.: 50474-320WO2 Genentech Docket No.: P38318-WO tiragolumab, wherein the gene signature score is based on the expression level of each of CCL5, ITGB1, BTG1, GZMK, LTB, IL7R, ZFP36L2, ITGA4, TXNIP, SLAMF6, HCST, ETS1, CXCR3, MS4A4A, DGKA, and YPEL3 detected in a sample from the individual; (e) an Ifit gene signature score that is at or above a reference gene signature score, thereby identifying the individual as one who may benefit from a treatment comprising atezolizumab and tiragolumab, wherein the gene signature score is based on the expression level of each of ISG15, IFIT1B, IFIT3, ISG20, IFI27L2, SAMHD1, ZBP1, SLFN5, IRF7, RTP4, USP18, PHF11, LGALS3BP, BST2, GBP2, IFITM3, STAT1, IFI16, and IFIH1 detected in a sample from the individual; (f) a Mitotic gene signature score that is at or above a reference gene signature score, thereby identifying the individual as one who may benefit from a treatment comprising atezolizumab and tiragolumab, wherein the gene signature score is based on the expression level of each of HSP90AB1, PTMA, XCL2, ODC1, TNFRSF9, ITM2A, MYC, YBX3, HSPA5, GPX1, RPS12, TUBA1B, MCM6, TUBB, MCM3, TPI1, MCM5, DUT, and FTL detected in a sample from the individual; (g) a Cytotox.2 gene signature score that is below a reference gene signature score, thereby identifying the individual as one who may benefit from a treatment comprising atezolizumab and tiragolumab, wherein the gene signature score is based on the expression level of each of HMGB2, TOP2A, MKI67, RRM2, PCLAF, TUBB, BIRC5, LMNB1, UBE2C, PTMA, STMN1, HMGN2, TUBA1B, LY6E, and DUT detected in a sample from the individual; or (h) a Cytotox.4 gene signature score that is below a reference gene signature score, thereby identifying the individual as one who may benefit from a treatment comprising atezolizumab and tiragolumab, wherein the gene signature score is based on the expression level of each of S100A6, NRN1, CXCR6, KLRC1, PDCD1, LGALS1, LAG3, ITGB1, ID2, LGALS3, NRGN, CST7, NKG7, S100A10, TNFRSF9, CD52, VIM, and IFITM2 detected in a sample from the individual.

104. The use of claim 103, wherein the gene signature score is an average of the expression levels of the members of the gene signature in the sample from the individual.

105. The use of claim 103 or 104, wherein the individual has been determined to have a Ccr7.3, Cxcr3, or Ccl5.1 gene signature score in the sample that is at or above a reference gene signature score and the benefit is a clinical response.

106. The use of claim 105, wherein the clinical response is a CR or a PR.

107. The use of claim 103 or 104, wherein the individual has been determined to have (i) a Ccr7.2, Cxcr3, Ifit, or Mitotic gene signature score in the sample that is at or above a reference gene signature score or (ii) a Cytotox.2 or Cytotox.4 gene signature score that is below a reference gene signature score and the benefit is an increase in OS HR.PATENT Attorney Docket No.: 50474-320WO2 Genentech Docket No.: P38318-WO 108. The use of claim 103 or 104, wherein the individual has been determined to have a Ccr7.2, Ccr7.3, or Cxcr3 gene signature score in the sample that is at or above a reference gene signature score and the benefit is an increase in OS.

109. The use of any one of claims 103-108, wherein the reference gene signature score is a pre- assigned gene signature score.

110. The use of any one of claims 103-109, wherein the reference gene signature score is a gene signature score in a reference population.

111. The use of claim 110, wherein the gene signature score in the reference population is the median Ccr7.2, Ccr7.3, Cxcr3, Ccl5.1, Ifit, Mitotic, Cytotox.2, or Cytotox.4 gene signature score in the reference population.

112. The use of claim 110 or 111, wherein the reference population is a population of individuals having the NSCLC.

113. Use of atezolizumab in the manufacture of a medicament for the treatment of an individual having a NSCLC, wherein the individual has been determined to have a gene signature score that is at or above a reference gene signature score, thereby identifying the individual as one who may benefit from a treatment comprising atezolizumab, wherein the gene signature score is based on the expression level of each of CCL5, CXCR3, and CXCR6 detected in a sample from the individual.

114. The use of claim 113, wherein the gene signature score is an average of the expression levels of CCL5, CXCR3, and CXCR6 in the sample from the individual.

115. The use of claim 113 or 114, wherein the expression level of CCR7 has been detected in the sample from the individual.

116. The use of claim 115, wherein the gene signature score is an average of the expression levels of CCL5, CXCR3, CXCR6, and CCR7 in the sample from the individual.

117. The use of any one of claims 113-116, wherein the benefit is an increase in progression-free survival (PFS) or OS.

118. The use of any one of claims 113-117, wherein the reference gene signature score is a pre- assigned gene signature score.

119. The use of any one of claims 113-118, wherein the reference gene signature score is a gene signature score in a reference population.PATENT Attorney Docket No.: 50474-320WO2 Genentech Docket No.: P38318-WO 120. The use of claim 119, wherein the gene signature score in the reference population is the median gene signature score based on the expression level of each of CCL5, CXCR3, and CXCR6 in the reference population.

121. The use of claim 119 or 120, wherein the reference population is a population of individuals having the NSCLC.

122. The use of any one of claims 113-121, wherein the treatment comprising atezolizumab is atezolizumab monotherapy.

123. The use of any one of claims 82-122, wherein the expression level is a nucleic acid expression level or a protein expression level.

124. The use of claim 123, wherein the expression level is a nucleic acid expression level.

125. The use of claim 124, wherein the nucleic acid expression level is determined by RNA-seq, RT- qPCR, qPCR, multiplex qPCR or RT-qPCR, microarray analysis, SAGE, MassARRAY technique, ISH, or a combination thereof.

126. The use of claim 124 or 125, wherein the nucleic acid expression level is an mRNA expression level.

127. The use of claim 126, wherein the mRNA expression level is determined by RNA-seq.

128. The use of claim 123, wherein the expression level is a protein expression level.

129. The use of claim 128, wherein the protein expression level is determined by mass spectrometry.

130. The use of any one of claims 82-129, wherein the sample is obtained from the individual prior to treatment with atezolizumab and / or tiragolumab.

131. The use of any one of claims 82-130, wherein the sample is a tissue sample, a tumor sample, a blood sample, a plasma sample, a serum sample, or a combination thereof.

132. The use of claim 131, wherein the sample is a tissue sample.

133. The use of claim 132, wherein the tissue sample is a tumor tissue sample.

134. The use of claim 133, wherein the tumor tissue sample is a biopsy.PATENT Attorney Docket No.: 50474-320WO2 Genentech Docket No.: P38318-WO 135. The use of claim 132, wherein the tissue sample is a tumor draining lymph node (dLN) sample.

136. The use of claim 131, wherein the sample is a blood sample.

137. The use of any one of claims 131-136, wherein the sample is an archival sample, a fresh sample, or a frozen sample.

138. The use of any one of claims 82-137, wherein the individual has a PD-L1-positive NSCLC.

139. The use of claim 138, wherein the PD-L1-positive NSCLC has been determined to have a PD- L1-positive tumor cell fraction by an immunohistochemical (IHC) assay.

140. The use of claim 139, wherein the PD-L1-positive tumor cell fraction is determined by positive staining with an anti-PD-L1 antibody, wherein the anti-PD-L1 antibody is SP263, 22C3, SP142, or 28-8.

141. The use of any one of claims 82-140, wherein the individual is a human.

142. The use of any one of claims 82-141, wherein the individual has not previously been treated for NSCLC.

143. Atezolizumab and / or tiragolumab for use in treating an individual having a NSCLC, wherein the individual has been determined to have an expression level of one or more of CCL5, CXCR3, CCR7, and CXCR6 in a sample from the individual that is at or above a reference expression level of CCL5, CXCR3, CCR7, or CXCR6, thereby identifying the individual as one who may benefit from a treatment comprising atezolizumab and tiragolumab.

144. The atezolizumab and / or tiragolumab for use of claim 143, wherein the benefit is a clinical response.

145. The atezolizumab and / or tiragolumab for use of claim 144, wherein the clinical response is a complete response (CR) or a partial response (PR).

146. The atezolizumab and / or tiragolumab for use of any one of claims 143-145, wherein the individual has been determined to have an expression level of one or more of CCL5, CXCR3, and CCR7 in the sample that is at or above a reference expression level of CCL5, CXCR3, or CCR7 and the benefit is an increase in overall survival (OS) hazard ratio (HR).

147. The atezolizumab and / or tiragolumab for use of any one of claims 143-146, wherein the individual has been determined to have an expression level of one or more of CCL5, CXCR3, andPATENT Attorney Docket No.: 50474-320WO2 Genentech Docket No.: P38318-WO CXCR6 in the sample that is at or above a reference expression level of CCL5, CXCR3, or CXCR6 and the benefit is an increase in overall survival (OS).

148. The atezolizumab and / or tiragolumab for use of any one of claims 143-147, wherein the reference expression level of CCL5, CXCR3, or CXCR6 is a pre-assigned expression level.

149. The atezolizumab and / or tiragolumab for use of any one of claims 143-148, wherein the reference expression level of CCL5, CXCR3, or CXCR6 is an expression level in a reference population.

150. The atezolizumab and / or tiragolumab for use of claim 149, wherein the expression level in the reference population is the median expression level of CCL5, CXCR3, or CXCR6 in the reference population.

151. The atezolizumab and / or tiragolumab for use of claim 149 or 150, wherein the reference population is a population of individuals having the NSCLC.

152. Atezolizumab and / or tiragolumab for use in treating an individual having a NSCLC, wherein the individual has been determined to have a gene signature score that is at or above a reference gene signature score, thereby identifying the individual as one who may benefit from a treatment comprising atezolizumab and tiragolumab, wherein the gene signature score is based on the expression level of each of CCL5, CXCR3, and CXCR6 detected in a sample from the individual.

153. The atezolizumab and / or tiragolumab for use of claim 152, wherein the gene signature score is an average of the expression levels of CCL5, CXCR3, and CXCR6 in the sample from the individual.

154. The atezolizumab and / or tiragolumab for use of claim 152 or 153, wherein the expression level of CCR7 has been detected in the sample from the individual.

155. The atezolizumab and / or tiragolumab for use of claim 154, wherein the gene signature score is an average of the expression levels of CCL5, CXCR3, CXCR6, and CCR7 in the sample from the individual.

156. The atezolizumab and / or tiragolumab for use of any one of claims 152-155, wherein the benefit is a clinical response.

157. The atezolizumab and / or tiragolumab for use of claim 156, wherein the clinical response is a CR or a PR.

158. The atezolizumab and / or tiragolumab for use of any one of claims 152-157, wherein the benefit is an increase in OS HR.PATENT Attorney Docket No.: 50474-320WO2 Genentech Docket No.: P38318-WO 159. The atezolizumab and / or tiragolumab for use of any one of claims 152-158, wherein the benefit is an increase in OS.

160. The atezolizumab and / or tiragolumab for use of any one of claims 152-159, wherein the reference gene signature score is a pre-assigned gene signature score.

161. The atezolizumab and / or tiragolumab for use of any one of claims 152-160, wherein the reference gene signature score is a gene signature score in a reference population.

162. The atezolizumab and / or tiragolumab for use of claim 161, wherein the gene signature score in the reference population is the median gene signature score based on the expression level of each of CCL5, CXCR3, and CXCR6 in the reference population.

163. The atezolizumab and / or tiragolumab for use of claim 161 or 162, wherein the reference population is a population of individuals having the NSCLC.

164. Atezolizumab and / or tiragolumab for use in treating an individual having a NSCLC, wherein the individual has been determined to have: (i) (a) a Ccr7.2 gene signature score that is at or above a reference gene signature score, thereby identifying the individual as one who may benefit from a treatment comprising atezolizumab and tiragolumab, wherein the gene signature score is based on the expression level of each of STAT1, LEF1, IRGM, CCR7, SELL, RPS24, RPS27, GBP2, RPS29, RPS3A, RPS20, KLF2, RPLP1, RPL13, DAPL1, SMC6, RFLNB, and RPS4X detected in a sample from the individual; (b) a Ccr7.3 gene signature score that is at or above a reference gene signature score, thereby identifying the individual as one who may benefit from a treatment comprising atezolizumab and tiragolumab, wherein the gene signature score is based on the expression level of each of DAPL1, CCR7, SMC4, RGCC, MXD4, CD8A, TCF7, ITGAE, RGS10, ZNRF1, CHD3, CD52, DDIT4, LEF1, IZUMO1R, INPP4B, and RFLNB detected in a sample from the individual; (c) a Cxcr3 gene signature score that is at or above a reference gene signature score, thereby identifying the individual as one who may benefit from a treatment comprising atezolizumab and tiragolumab, wherein the gene signature score is based on the expression level of each of CXCR6, CKB, GIMAP5, ID2, LTB, FGL2, RAMP1, LYST, ASB2, IL2RB, CXCR3, SERINC3, INPP4B, ANXA1, XCL2, SOCS2, CD82, CD4, and GIMAP7 detected in a sample from the individual; (d) a Ccl5.1 gene signature score that is at or above a reference gene signature score, thereby identifying the individual as one who may benefit from a treatment comprising atezolizumab and tiragolumab, wherein the gene signature score is based on the expression level of each of CCL5, ITGB1, BTG1, GZMK, LTB, IL7R, ZFP36L2, ITGA4, TXNIP, SLAMF6, HCST, ETS1, CXCR3, MS4A4A, DGKA, and YPEL3 detected in a sample from the individual;PATENT Attorney Docket No.: 50474-320WO2 Genentech Docket No.: P38318-WO (e) an Ifit gene signature score that is at or above a reference gene signature score, thereby identifying the individual as one who may benefit from a treatment comprising atezolizumab and tiragolumab, wherein the gene signature score is based on the expression level of each of ISG15, IFIT1B, IFIT3, ISG20, IFI27L2, SAMHD1, ZBP1, SLFN5, IRF7, RTP4, USP18, PHF11, LGALS3BP, BST2, GBP2, IFITM3, STAT1, IFI16, and IFIH1 detected in a sample from the individual; (f) a Mitotic gene signature score that is at or above a reference gene signature score, thereby identifying the individual as one who may benefit from a treatment comprising atezolizumab and tiragolumab, wherein the gene signature score is based on the expression level of each of HSP90AB1, PTMA, XCL2, ODC1, TNFRSF9, ITM2A, MYC, YBX3, HSPA5, GPX1, RPS12, TUBA1B, MCM6, TUBB, MCM3, TPI1, MCM5, DUT, and FTL detected in a sample from the individual; (g) a Cytotox.2 gene signature score that is below a reference gene signature score, thereby identifying the individual as one who may benefit from a treatment comprising atezolizumab and tiragolumab, wherein the gene signature score is based on the expression level of each of HMGB2, TOP2A, MKI67, RRM2, PCLAF, TUBB, BIRC5, LMNB1, UBE2C, PTMA, STMN1, HMGN2, TUBA1B, LY6E, and DUT detected in a sample from the individual; or (h) a Cytotox.4 gene signature score that is below a reference gene signature score, thereby identifying the individual as one who may benefit from a treatment comprising atezolizumab and tiragolumab, wherein the gene signature score is based on the expression level of each of S100A6, NRN1, CXCR6, KLRC1, PDCD1, LGALS1, LAG3, ITGB1, ID2, LGALS3, NRGN, CST7, NKG7, S100A10, TNFRSF9, CD52, VIM, and IFITM2 detected in a sample from the individual.

165. The atezolizumab and / or tiragolumab for use of claim 164, wherein the gene signature score is an average of the expression levels of the members of the gene signature in the sample from the individual.

166. The atezolizumab and / or tiragolumab for use of claim 164 or 165, wherein the individual has been determined to have a Ccr7.3, Cxcr3, or Ccl5.1 gene signature score in the sample that is at or above a reference gene signature score and the benefit is a clinical response.

167. The atezolizumab and / or tiragolumab for use of claim 166, wherein the clinical response is a CR or a PR.

168. The atezolizumab and / or tiragolumab for use of claim 164 or 165, wherein the individual has been determined to have (i) a Ccr7.2, Cxcr3, Ifit, or Mitotic gene signature score in the sample that is at or above a reference gene signature score or (ii) a Cytotox.2 or Cytotox.4 gene signature score that is below a reference gene signature score and the benefit is an increase in OS HR.

169. The atezolizumab and / or tiragolumab for use of claim 164 or 165, wherein the individual has been determined to have a Ccr7.2, Ccr7.3, or Cxcr3 gene signature score in the sample that is at or above a reference gene signature score and the benefit is an increase in OS.PATENT Attorney Docket No.: 50474-320WO2 Genentech Docket No.: P38318-WO 170. The atezolizumab and / or tiragolumab for use of any one of claims 164-169, wherein the reference gene signature score is a pre-assigned gene signature score.

171. The atezolizumab and / or tiragolumab for use of any one of claims 164-170, wherein the reference gene signature score is a gene signature score in a reference population.

172. The atezolizumab and / or tiragolumab for use of claim 171, wherein the gene signature score in the reference population is the median Ccr7.2, Ccr7.3, Cxcr3, Ccl5.1, Ifit, Mitotic, Cytotox.2, or Cytotox.4 gene signature score in the reference population.

173. The atezolizumab and / or tiragolumab for use of claim 171 or 172, wherein the reference population is a population of individuals having the NSCLC.

174. Atezolizumab for use in treating an individual having a NSCLC, wherein the individual has been determined to have a gene signature score that is at or above a reference gene signature score, thereby identifying the individual as one who may benefit from a treatment comprising atezolizumab, wherein the gene signature score is based on the expression level of each of CCL5, CXCR3, and CXCR6 detected in a sample from the individual.

175. The atezolizumab for use of claim 174, wherein the gene signature score is an average of the expression levels of CCL5, CXCR3, and CXCR6 in the sample from the individual.

176. The atezolizumab for use of claim 174 or 175, wherein the expression level of CCR7 has been detected in the sample from the individual.

177. The atezolizumab for use of claim 176, wherein the gene signature score is an average of the expression levels of CCL5, CXCR3, CXCR6, and CCR7 in the sample from the individual.

178. The atezolizumab for use of any one of claims 174-177, wherein the benefit is an increase in progression-free survival (PFS) or OS.

179. The atezolizumab for use of any one of claims 174-178, wherein the reference gene signature score is a pre-assigned gene signature score.

180. The atezolizumab for use of any one of claims 174-179, wherein the reference gene signature score is a gene signature score in a reference population.PATENT Attorney Docket No.: 50474-320WO2 Genentech Docket No.: P38318-WO 181. The atezolizumab for use of claim 180, wherein the gene signature score in the reference population is the median gene signature score based on the expression level of each of CCL5, CXCR3, and CXCR6 in the reference population.

182. The atezolizumab for use of claim 180 or 181, wherein the reference population is a population of individuals having the NSCLC.

183. The atezolizumab for use of any one of claims 174-182, wherein the treatment comprising atezolizumab is atezolizumab monotherapy.

184. The atezolizumab and / or tiragolumab for use of any one of claims 143-183, wherein the expression level is a nucleic acid expression level or a protein expression level.

185. The atezolizumab and / or tiragolumab for use of claim 184, wherein the expression level is a nucleic acid expression level.

186. The atezolizumab and / or tiragolumab for use of claim 185, wherein the nucleic acid expression level is determined by RNA-seq, RT-qPCR, qPCR, multiplex qPCR or RT-qPCR, microarray analysis, SAGE, MassARRAY technique, ISH, or a combination thereof.

187. The atezolizumab and / or tiragolumab for use of claim 185 or 186, wherein the nucleic acid expression level is an mRNA expression level.

188. The atezolizumab and / or tiragolumab for use of claim 187, wherein the mRNA expression level is determined by RNA-seq.

189. The atezolizumab and / or tiragolumab for use of claim 184, wherein the expression level is a protein expression level.

190. The atezolizumab and / or tiragolumab for use of claim 189, wherein the protein expression level is determined by mass spectrometry.

191. The atezolizumab and / or tiragolumab for use of any one of claims 143-190, wherein the sample is obtained from the individual prior to treatment with atezolizumab and / or tiragolumab.

192. The atezolizumab and / or tiragolumab for use of any one of claims 143-191, wherein the sample is a tissue sample, a tumor sample, a blood sample, a plasma sample, a serum sample, or a combination thereof.PATENT Attorney Docket No.: 50474-320WO2 Genentech Docket No.: P38318-WO 193. The atezolizumab and / or tiragolumab for use of claim 192, wherein the sample is a tissue sample.

194. The atezolizumab and / or tiragolumab for use of claim 193, wherein the tissue sample is a tumor tissue sample.

195. The atezolizumab and / or tiragolumab for use of claim 194, wherein the tumor tissue sample is a biopsy.

196. The atezolizumab and / or tiragolumab for use of claim 193, wherein the tissue sample is a tumor draining lymph node (dLN) sample.

197. The atezolizumab and / or tiragolumab for use of claim 192, wherein the sample is a blood sample.

198. The atezolizumab and / or tiragolumab for use of any one of claims 192-197, wherein the sample is an archival sample, a fresh sample, or a frozen sample.

199. The atezolizumab and / or tiragolumab for use of any one of claims 143-198, wherein the individual has a PD-L1-positive NSCLC.

200. The atezolizumab and / or tiragolumab for use of claim 199, wherein the PD-L1-positive NSCLC has been determined to have a PD-L1-positive tumor cell fraction by an immunohistochemical (IHC) assay.

201. The atezolizumab and / or tiragolumab for use of claim 200, wherein the PD-L1-positive tumor cell fraction is determined by positive staining with an anti-PD-L1 antibody, wherein the anti-PD-L1 antibody is SP263, 22C3, SP142, or 28-8.

202. The atezolizumab and / or tiragolumab for use of any one of claims 143-201, wherein the individual is a human.

203. The atezolizumab and / or tiragolumab for use of any one of claims 143-202, wherein the individual has not previously been treated for NSCLC.

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