Bcl6 bifunctional degraders

Abstract

This disclosure provides compounds of Formula (I) (e.g., Formula (I-a), (I-a1), (I-b), or (I-c)), or pharmaceutically acceptable salts thereof, that induce degradation of a BCL6 protein. These compounds are useful, for example, for treating a cancer in a subject (e.g., a human). This disclosure also provides compositions containing compounds of Formula (I) (e.g., Formula (I-a), (I-a1), (I-b), or (I-c)), or pharmaceutically acceptable salts thereof, as well as methods of using and making the same

Description

[0001] BCL6 Bifunctional Degraders CROSS REFERENCE TO RELATED APPLICATIONS This application claims priority to U.S. Provisional Application Serial Nos.63 / 580,215, filed September 1, 2023; 63 / 607,012, filed December 6, 2023; 63 / 624,171, filed January 23, 2024; and 63 / 665,670, filed June 28, 2024; each of which is hereby incorporated by reference in its entirety. 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 file, created on August 26, 2024, is named TLS-055WO_SL.xml and is 2,665 bytes in size. TECHNICAL FIELD This disclosure provides compounds of Formula (I) (e.g., Formula (I-a), (I-a1), (I-b), or (I-c)), or pharmaceutically acceptable salts thereof, that induce degradation of a BCL6 protein. These compounds are useful, for example, for treating cancer in a subject (e.g., a human). This disclosure also provides compositions containing compounds of Formula (I) (e.g., Formula (I-a), (I-a1), (I-b), or (I-c)), or pharmaceutically acceptable salts thereof, as well as methods of using and making the same. BACKGROUND B-cell lymphoma 6 (BCL6) protein is a transcriptional repressor involved in the formation and maintenance of germinal centers (GCs) within lymphoid follicles. It controls the functions of the GC and coordinates the activities of signaling mediators in the maturation of GC B cells. There are over 1000 known or putative BCL6 target genes, including MYC, BCL2, genes related to DNA damage response (e.g., ATR, TP53), and cell cycle checkpoint control (e.g., CDKN1A, CDKN1B). BCL6 is expressed in the dark zone cells of GCs, where somatic hypermutation is allowed to occur to generate high-affinity B-cell receptors. Overexpression or loss of control of BCL6, for example by translocation, can permit maintenance of the pro- hypermutation functions and abrogation of the antitumor functions of BCL6. SUMMARY Provided herein are compounds of Formula (I): Formula (I) or pharmaceutically acceptable salts thereof, wherein: TBM is selected from the group consisting of: (T1) and (T2): wherein X1, X3, m3, R1, R2a, R4, R5, R6, Xa, L, Ring C, and X are as defined herein. Also provided herein are pharmaceutical compositions comprising a compound of Formula (I) (e.g., Formula (I-a), (I-a1), (I-b), or (I-c)), or a pharmaceutically acceptable salt thereof, and a pharmaceutically acceptable carrier. Provided herein are methods for treating cancer in a subject in need thereof, the methods comprising administering to the subject a therapeutically effective amount of a compound of Formula (I) (e.g., Formula (I-a), (I-a1), (I-b), or (I-c)), or a pharmaceutically acceptable salt thereof, or a pharmaceutical composition as provided herein. Also provided herein are BCL6 proteins non-covalently bound with a compound of Formula (I) (e.g., Formula (I-a), (I-a1), (I-b), or (I-c)), or a pharmaceutically acceptable salt thereof. Also provided herein are ternary complexes comprising a BCL6 protein, a compound of Formula (I) (e.g., Formula (I-a), (I-a1), (I-b), or (I-c)), or a pharmaceutically acceptable salt thereof, and a cereblon (CRBN) E3 ligase protein (also referred to herein as a CRBN protein), or a portion thereof. To facilitate understanding of the disclosure set forth herein, a number of additional terms are provided. Generally, the nomenclature used herein and the laboratory procedures in organic chemistry, medicinal chemistry, and pharmacology described are those well-known and commonly employed in the art. Unless defined otherwise, all technical and scientific terms used herein generally have the same meaning as commonly understood by one of ordinary skill in the art to which this disclosure belongs. Each of the patents, applications, published applications, and other publications that are mentioned throughout the specification and the attached appendices are incorporated herein by reference in their entireties. In the case of conflict between the present disclosure and any content incorporated by reference, the present disclosure controls. The details of one or more embodiments of the invention are set forth in the accompanying drawings and the description below. Other features and advantages of the invention will be apparent from the description and drawings, and from the claims. DETAILED DESCRIPTION This disclosure provides compounds of Formula (I) (e.g., Formula (I-a), (I-a1), (I-b), or (I-c)), or pharmaceutically acceptable salts thereof, that induce degradation of a BCL6 protein. These compounds are useful, e.g., for treating a cancer. This disclosure also provides compositions containing compounds of Formula (I) (e.g., Formula (I-a), (I-a1), (I-b), or (I- c)), or pharmaceutically acceptable salts thereof, as well as methods of using and making the same. Upon antigen challenge, germinal centers (GCs) are formed in lymphoid follicles, and B-cells in the dark zone of GCs undergo rapid proliferation and somatic hypermutation, both of their immunoglobin variable genes to generate high-affinity B-cell receptors, as well as of other genes including BCL6. BCL6 is often considered to be a ‘master regulator’ of the GC reaction. In some cancers, BCL6 can be mutated, translocated, and / or BCL6 expression can be upregulated. See, e.g., Leeman-Neill and Bhagat, Expert Opinion on Therapeutic Targets 22.2 (2018): 143-152, doi: 10.1080 / 14728222.2018.1420782; Mlynarczyk and Melnick. Immunological Reviews 288.1 (2019): 214-239, doi: 10.1111 / imr.12755. The BCL6 protein has multiple domains, including a BTB domain, an RD2 domain, and a DNA binding domain. The N-terminal BTB domain is the site of homodimerization of BCL6, and the interface of the monomers forms the “lateral groove”, which is a binding site for endogenous co-repressors of BCL6, such as SMRT, NCOR, and BCOR. See, e.g., Cardenas, Mariano G., et al. Clinical Cancer Research 23.4 (2017): 885-893, doi: 10.1158 / 1078- 0432.CCR-16-2071. Compounds that induce degradation of a target protein are sometimes referred to as heterobifunctional compounds, PROTACs, or degraders. Such compounds generally include a moiety that binds to the target protein and a moiety that binds to a ubiquitin E3 ligase (sometimes referred to as an E3 ligase or simply an E3), these two moieties being optionally separated by a linker. To induce degradation, heterobifunctional compounds are believed to induce formation of a ternary complex between the target protein, the compound, and an E3 ligase. Formation of the ternary complex is then followed by ubiquitination of the target protein and degradation of the ubiquitinated target protein by a proteosome. Several E3 ligases have been used as the partner E3 ligase for heterobifunctional degraders. Herein, the cereblon (CRBN) E3 ligase (also referred to herein as a CRBN protein) is used. A degradation approach for a target protein can have potential advantages compared to, e.g., small molecule inhibition of the target protein. One potential advantage is that the duration of effect of a heterobifunctional compound is generally based on the resynthesis rate of the target protein. Another potential advantage is that many heterobifunctional compounds are believed to be released from the ubiquitinated target protein-E3 ligase complex and made available for formation of further ternary complexes; this is sometimes referred to as “catalytic” turnover of the heterobifunctional compound. Degradation of a target protein can also be advantageous over small molecule inhibition in some cases, as degradation can impair a scaffolding function of a target protein, whereas a small molecule might not. It is also generally believed that for formation of a ternary complex, high affinity to the target protein is not always required. Heterobifunctional compounds are further described in, for example, International Publication Nos. WO 2021 / 077010; WO 2022 / 221673; WO 2023 / 212147; WO 2024 / 151557; WO 2023 / 114460; McCoull, William, et al., ACS Chemical Biology 13.11 (2018): 3131-3141, doi: 10.1021 / acschembio.8b00698; Chamberlain and Hamann, Nature Chemical Biology 15.10 (2019): 937-944, doi: 10.1038 / s41589-019-0362-y; Li and Song, Journal of Hematology & Oncology 13 (2020), doi: 10.1186 / s13045-020-00885-3; Wu, et al. Nature Structural & Molecular Biology 27.7 (2020): 605-614, doi: 10.1038 / s41594-020-0438-0; Dong, et al., Journal of Medicinal Chemistry 64.15 (2021): 10606-10620, doi: 10.1021 / acs.jmedchem.1c00895; Yang, et al., Targeted Oncology 16.1 (2021): 1-12, doi: 10.1007 / s11523-020-00782-2. Compound Embodiments Provided herein are compounds of Formula (I): Formula (I) or pharmaceutically acceptable salts thereof, wherein: TBM is selected from the group consisting of: (T1) and (T2): X1is C2-6 alkylene optionally substituted with 1-3 Rc, wherein a CH2 group of the C2-6 alkylene is optionally replaced with X2; X2is selected from the group consisting of: -O-, -N(Rd)-, and -S(O)0-2-; m3 is 0 or 1; X3is C1-3 alkylene optionally substituted with 1-3 Rc; R1is selected from the group consisting of: H, halo, and Rb1; R2ais selected from the group consisting of: H, halo, cyano, C1-3 alkyl, C1-3 haloalkyl, C1-3alkoxy, and C1-3haloalkoxy; each R4is independently selected from the group consisting of: H, C1-3 alkyl, and C1-3 haloalkyl; R5is selected from the group consisting of: -OH, -NH2, -R5A, -OR5A, and -NR5ARf, wherein: R5Ais selected from the group consisting of: C1-6alkyl optionally substituted with 1-3 Rc; and -(C0-3 alkylene)-Rb1, wherein the C0-3 alkylene is optionally substituted with 1-2 Rc; Xais selected from the group consisting of: N and CRXa; R6and RXaare independently selected from the group consisting of: H, halo, C1-2 alkyl, C1-2 haloalkyl, C1-2 alkoxy, CN, and -C≡CH; L is –(LA)n1–, attached to aa or bb, wherein: n1 is an integer from 1 to 5; and each LAis independently selected from the group consisting of: LA1, LA3, and LA4, wherein: 0-2 of LAis LA1; 0-2 of LAis LA3; and 1-3 of LAis LA4, each LA1is independently selected from the group consisting of: -CH2-, -CHRL-, and - C(RL)2-, wherein: each RLis independently selected from the group consisting of: halo, cyano, -OH, -C1-6 alkoxy, -C1-6 haloalkoxy, -(C0-3 alkylene)-(C3-5 cycloalkyl), -(C0-3 alkylene)-(4-6 membered heterocyclyl), and C1-6 alkyl optionally substituted with 1-6 Rc; each LA3is independently selected from the group consisting of: -N(Rd)-, -N(Rb)-, -O- , -S(O)0-2-, and C(=O); each LA4is independently selected from the group consisting of: (a) C3-15 cycloalkylene or 4-15 membered heterocyclylene, each of which is optionally substituted with 1-6 substituents independently selected from the group consisting of: Raand Rb; and (b) phenylene or 5-6 membered heteroarylene, each of which is optionally substituted with 1-3 substituents independently selected from the group consisting of: Raand Rb; Ring C is selected from the group consisting of: , wherein: c1 is 0, 1, or 2; each RYbis independently selected from the group consisting of Raand Rb; RYais selected from the group consisting of: H, Ra, and Rb; and yy represents the point of attachment to L; X is CH or N; each Rais independently selected from the group consisting of: (a) halo; (b) cyano; (c) -OH; (d) oxo; (e) C1-6 alkoxy optionally substituted with 1-6 Rc; (f) -NRdRe; (g) C(=O)C1-6alkyl; (h) C(=O)OC1-6 alkyl; (i) C(=O)N(Rf)2; (j) S(O)0-2(C1-6alkyl); (k) S(O)0-2(C1-6 haloalkyl); and (l) C1-6 alkyl, C2-6 alkenyl, or C2-6 alkynyl, each optionally substituted with 1-6 Rc; each Rbis independently selected from the group consisting of: -(Lb)b-Rb1and -Rb1, wherein: each b is independently 1, 2, or 3; each Lbis independently selected from the group consisting of: -O-, -N(H)-, -N(C1-3alkyl)-, -S(O)0-2-, C(=O), and C1-3 alkylene; and each Rb1is independently selected from the group consisting of: C3-6cycloalkyl and 4- 8 membered heterocyclyl, each of which is optionally substituted with 1-3 Rg; each Rcis independently selected from the group consisting of: halo, cyano, -OH, -C1-6alkoxy, -C1-6haloalkoxy, -NRdRe, C(=O)C1-6alkyl, C(=O)OC1-6alkyl, C(=O)N(Rf)2, S(O)0-2(C1-6 alkyl), and S(O)0-2(C1-6 haloalkyl); each Rdand Reis independently selected from the group consisting of: H, C(=O)C1-6 alkyl, C(=O)C1-6haloalkyl, C(=O)OC1-6alkyl, C(=O)OC1-6haloalkyl, C(=O)N(Rf)2, S(O)1-2(C1-6alkyl), S(O)1-2(C1-6haloalkyl), S(O)1-2N(Rf)2, and C1-6alkyl optionally substituted with 1-3 Rh; each Rfis independently selected from the group consisting of: H and C1-6 alkyl optionally substituted with 1-3 Rh; each Rgis independently selected from the group consisting of: Rh, oxo, C1-3 alkyl, and C1-3 haloalkyl; and each Rhis independently selected from the group consisting of: halo, cyano, -OH, -(C0-3 alkylene)-C1-6 alkoxy, -(C0-3 alkylene)-C1-6 haloalkoxy, -(C0-3 alkylene)-NH2, -(C0-3 alkylene)-N(H)(C1-3 alkyl), and –(C0-3 alkylene)-N(C1-3 alkyl)2. Certain combinations of heteroatoms (e.g., N, O, S, or halo) define compounds which are less stable under physiological conditions. Examples include (1) compounds containing acetal or animal linkages; (2) compounds containing acyclic N-O, N-N, or N-S(O)0 bonds; and (3) compounds containing O-O, O-S(O)0-2, N-halo, O-halo, and S(O)0-2-halo bonds. Accordingly, such compounds are less preferred. As used herein, “acyclic bonds” mean chemical bonds that are not part of a ring. Examples include the N-O bond i . avoidance of doubt, acyclic N-O, N- N, or N-S(O)0 bonds (i.e., those bonds that are not part of a ring (e.g., in or )) are less preferred, but Formula (I) compounds can include N-O, N-N, or N-S(O)0bonds that form part of a ring (e.g., the N-N bond i In some embodiments of Formula (I), TBM is selected from the group consisting of: (T1) and (T2): X1is C2-6alkylene optionally substituted with 1-3 Rc, wherein a CH2group of the C2-6alkylene is optionally replaced with X2; X2is selected from the group consisting of: -O-, -N(Rd)-, and -S(O)0-2-; m3 is 0 or 1; X3is C1-3 alkylene optionally substituted with 1-3 Rc; R1is selected from the group consisting of: H and halo R2ais selected from the group consisting of: H, halo, cyano, C1-3alkyl, C1-3haloalkyl, C1-3 alkoxy, and C1-3 haloalkoxy; each R4is independently selected from the group consisting of: H, C1-3alkyl, and C1-3haloalkyl; R5is selected from the group consisting of: -OH, -NH2, -R5A, -OR5A, and -NR5ARf, wherein: R5Ais selected from the group consisting of: C1-6alkyl optionally substituted with 1-3 Rc; and -(C0-3 alkylene)-Rb1, wherein the C0-3 alkylene is optionally substituted with 1-2 Rc; Xais selected from the group consisting of: N and CRXa; R6and RXaare independently selected from the group consisting of: H, halo, C1-2 alkyl, C1-2 haloalkyl, C1-2 alkoxy, CN, and -C≡CH; L is –(LA)n1–, attached to aa or bb, wherein: n1 is an integer from 1 to 5; and each LAis independently selected from the group consisting of: LA1, LA3, and LA4, wherein: 0-2 of LAis LA1; 0-2 of LAis LA3; and 1-3 of LAis LA4, each LA1is independently selected from the group consisting of: -CH2-, -CHRL-, and - C(RL)2-, wherein: each RLis independently selected from the group consisting of: halo, cyano, -OH, -C1- 6 alkoxy, -C1-6 haloalkoxy, -(C0-3 alkylene)-(C3-5 cycloalkyl), -(C0-3 alkylene)-(4-6 membered heterocyclyl), and C1-6alkyl optionally substituted with 1-6 Rc; each LA3is independently selected from the group consisting of: -N(Rd)-, -N(Rb)-, -O- , -S(O)0-2-, and C(=O); each LA4is independently selected from the group consisting of: (a) C3-15 cycloalkylene or 4-15 membered heterocyclylene, each of which is optionally substituted with 1-6 substituents independently selected from the group consisting of: Raand Rb; and (b) phenylene or 5-6 membered heteroarylene, each of which is optionally substituted with 1-3 substituents independently selected from the group consisting of: Raand Rb; Ring C is selected from the group consisting of: , wherein: c1 is 0, 1, or 2; each RYaand RYbis independently selected from the group consisting of Raand Rb; and yy represents the point of attachment to L; X is CH or N; each Rais independently selected from the group consisting of: (a) halo; (b) cyano; (c) -OH; (d) oxo; (e) C1-6 alkoxy optionally substituted with 1-6 Rc; (f) -NRdRe; (g) C(=O)C1-6 alkyl; (h) C(=O)OC1-6 alkyl; (i) C(=O)N(Rf)2; (j) S(O)0-2(C1-6alkyl); (k) S(O)0-2(C1-6 haloalkyl); and (l) C1-6 alkyl, C2-6 alkenyl, or C2-6 alkynyl, each optionally substituted with 1-6 Rc; each Rbis independently selected from the group consisting of: -(Lb)b-Rb1and -Rb1, wherein: each b is independently 1, 2, or 3; each Lbis independently selected from the group consisting of: -O-, -N(H)-, -N(C1-3 alkyl)-, -S(O)0-2-, C(=O), and C1-3 alkylene; and each Rb1is independently selected from the group consisting of: C3-6cycloalkyl and 4- 8 membered heterocyclyl, each of which is optionally substituted with 1-3 Rg; each Rcis independently selected from the group consisting of: halo, cyano, -OH, -C1-6alkoxy, -C1-6haloalkoxy, -NRdRe, C(=O)C1-6alkyl, C(=O)OC1-6alkyl, C(=O)N(Rf)2, S(O)0-2(C1-6 alkyl), and S(O)0-2(C1-6 haloalkyl); each Rdand Reis independently selected from the group consisting of: H, C(=O)C1-6 alkyl, C(=O)C1-6haloalkyl, C(=O)OC1-6alkyl, C(=O)OC1-6haloalkyl, C(=O)N(Rf)2, S(O)1-2(C1-6 alkyl), S(O)1-2(C1-6 haloalkyl), S(O)1-2N(Rf)2, and C1-6 alkyl optionally substituted with 1-3 Rh; each Rfis independently selected from the group consisting of: H and C1-6alkyl optionally substituted with 1-3 Rh; each Rgis independently selected from the group consisting of: Rh, oxo, C1-3 alkyl, and C1-3 haloalkyl; and each Rhis independently selected from the group consisting of: halo, cyano, -OH, -(C0-3 alkylene)-C1-6 alkoxy, -(C0-3 alkylene)-C1-6 haloalkoxy, -(C0-3 alkylene)-NH2, -(C0-3 alkylene)-N(H)(C1-3 alkyl), and –(C0-3 alkylene)-N(C1-3 alkyl)2. In some embodiments of Formula (I), the TBM is (T1). In some embodiments of Formula (I), the TBM is (T1a): wherein X1ais a C1-4 alkylene optionally substituted with 1-3 Rc. In some embodiments of Formula (I), the TBM is (T1a-1): wherein X1ais C2-4 alkylene optionally substituted with 1-3 Rc. In some embodiments of Formula (I), the TBM is (T1a-2): wherein RX1is methyl or H. In some embodiments of Formula (I), each R4is H. In some embodiments of Formula (I), R5is -NR5ARf. In some such embodiments, R5Ais C1-3 alkyl. For example, R5can be -NH(Me). In some embodiments of Formula (I), the TBM is (T1a-1a): wherein RX1is methyl or H. In some embodiments of Formula (I), the TBM is (T2). In some embodiments of Formula (I), the TBM is (T2-a): wherein m3 is 1; X3is C1-3 alkylene; and R1is H. In some embodiments of Formula (I), R2ais H. In some embodiments of Formula (I), Xais N. In some embodiments of Formula (I), R6is halo. For example, R6can be -Cl. In some embodiments of Formula (I), L is –(LA)n1–, wherein: n1 is an integer from 2 to 4; and each LAis independently selected from the group consisting of: LA1, LA3, and LA4, wherein: 0-2 of LAis LA1; 0-2 of LAis LA3; and 2-3 of LAare LA4, wherein: each LA4is independently a C3-10cycloalkylene or a 4-12 membered heterocyclylene, each of which is optionally substituted with 1-3 Ra, wherein: each Rapresent on LA4is independently selected from the group consisting of: -F, CN, C1-3alkoxy, OH, and C1-3alkyl optionally substituted with 1-3 F; and each RLis independently selected from the group consisting of: -F, -OH, and C1-3 alkyl optionally substituted with 1-3 Rc(e.g., C1-3 alkyl optionally substituted with 1-3 -F). In some embodiments of Formula (I), L is –(LA)n1–, wherein: n1 is an integer from 2 to 4; and each LAis independently selected from the group consisting of: LA1and LA4, wherein: 0-2 of LAis LA1; and 2-3 of LAare LA4, wherein: each LA4is independently a 4-12 membered heterocyclylene, each of which is optionally substituted with 1-3 Ra, wherein: each Rapresent on LA4is independently selected from the group consisting of: -F, CN, C1-3 alkoxy, OH, and C1-3 alkyl optionally substituted with 1-3 F; and each RLis independently selected from the group consisting of: -F, -OH, and C1-3alkyl optionally substituted with 1-3 Rc(e.g., C1-3 alkyl optionally substituted with 1-3 -F). In some embodiments of Formula (I), L is -LA4a-LA1-LA4b-bb, wherein: LA4aand LA4bare each an independently selected LA4, and bb represents the point of attachment to Ring C. In some embodiments, LA4aand LA4bare independently a 4-12 membered nitrogen- containing heterocyclylene optionally substituted with 1-3 Ra; and each RLis independently selected from the group consisting of: -F, -OH, and C1-3alkyl optionally substituted with 1-3 Rc(e.g., C1-3 alkyl optionally substituted with 1-3 -F). In some embodiments, LA4aand LA4beach contain 1-2 ring nitrogen atoms and no additional ring heteroatoms. In some embodiments, each Rapresent on LA4aand / or LA4bis independently selected from the group consisting of: -F and C1-3 alkyl optionally substituted with 1-3 F (e.g., -CH3). In some embodiments, LA4aand LA4bare each an independently selected monocyclic 4-6 membered nitrogen-containing heterocyclylene optionally substituted with 1-3 Ra. In some embodiments, one of LA4aand LA4bis a 1,4-piperidinylene; and the other of LA4aand LA4bis independently selected from the group consisting of: 1,4-piperidinylene and 1,4- piperazinylene, wherein each of the 1,4-piperidinylene or 1,4-piperazinylene is optionally substituted with 1-2 Ra. In some embodiments, LA4aand LA4beach contain 1-2 ring nitrogen atoms and no additional ring heteroatoms. In some embodiments, each Rapresent on LA4aand / or LA4bis independently selected from the group consisting of: -F and C1-3 alkyl optionally substituted with 1-3 F (e.g., -CH3). In some embodiments, one of LA4aand LA4bis a monocyclic 4-6 membered nitrogen- containing heterocyclylene optionally substituted with 1-3 Ra; and the other of LA4aand LA4bis a bicyclic spirocyclic 6-12 (e.g., 10-12) membered nitrogen-containing heterocyclylene optionally substituted with 1-3 Ra. In some embodiments, LA4bis a monocyclic 4-6 membered nitrogen-containing heterocyclylene optionally substituted with 1-3 Ra; and LA4ais a bicyclic spirocyclic 6-12 (e.g., 10-12) membered nitrogen-containing heterocyclylene optionally substituted with 1-3 Ra. In some embodiments, LA4bis 1,4-piperidinylene optionally substituted with 1-2 Ra; and LA4ais a bicyclic spirocyclic 10-12 membered nitrogen-containing heterocyclylene optionally substituted with 1-2 Ra. In some embodiments, LA4aand LA4beach contain 1-2 ring nitrogen atoms and no additional ring heteroatoms. In some embodiments, each Rapresent on LA4aand / or LA4bis independently selected from the group consisting of: - F and C1-3 alkyl optionally substituted with 1-3 F (e.g., -CH3). In some embodiments of Formula (I), LA1is -CH2-. In some embodiments of Formula (I), LA1is -CHRL-, wherein RLis C1-3 alkyl optionally substituted with 1-3 F (e.g., RLis -CH3). In some embodiments of Formula (I), Ring C is selected from the group consisting of: . In some embodiments of Formula (I), Ring C is selected from the group consisting of: In some embodiments of Formula (I), RYais C1-6alkyl optionally substituted with 1-3 Rc; and each RYbis independently selected from the group consisting of: -F and C1-3 alkyl optionally substituted with 1-3 -F. In some embodiments of Formula (I), each RYbis -F. In some embodiments of Formula (I), RYais C1-3 alkyl optionally substituted with 1-3 -F, and each RYbis -F. In some embodiments of Formula (I), RYais methyl. In some embodiments of Formula (I), RYais methyl; and each RYbis -F. In some embodiments of Formula (I), Ring C is selected from the group consisting of: In some embodiments of Formula (I), is X is CH. In some embodiments, the compounds of Formula (I) are compounds of Formula (I-a): Formula (I-a) or pharmaceutically acceptable salts thereof, wherein: X1ais C2-4alkylene optionally substituted with 1-3 Rc; LA4aand LA4bare independently a 4-12 membered nitrogen-containing heterocyclylene optionally substituted with 1-3 Ra; LA1is CH2or CHRL, RLis selected from the group consisting of: -F, -OH, and C1-3alkyl optionally substituted with 1-3 Rc(e.g., C1-3 alkyl optionally substituted with 1-3 -F); Ring C is selected from the group consisting of: . c1 is 0, 1, or 2; RYais C1-6 alkyl optionally substituted with 1-3 Rc; each RYbis independently selected from the group consisting of: -F and C1-3alkyl optionally substituted with 1-3 -F; and yy represents the point of attachment to LA4b. In some embodiments of Formula (I-a), each R4is H. In some embodiments of Formula (I-a), R5is -NR5ARf. In some embodiments, R5Ais C1-3 alkyl. For example, R5can be -NH(Me). In some embodiments, the compounds of Formula (I) are compounds of Formula (I- a1): Formula (I-a1) or pharmaceutically acceptable salts thereof, wherein: RX1is methyl or H; LA4aand LA4bare independently a 4-12 membered nitrogen-containing heterocyclylene optionally substituted with 1-3 Ra; LA1is CH2or CHRL, RLis selected from the group consisting of: -F, -OH, and C1-3alkyl optionally substituted with 1-3 Rc(e.g., C1-3 alkyl optionally substituted with 1-3 -F); each Rapresent on LA4aand / or LA4bis independently selected from the group consisting of: -F, CN, C1-3alkoxy, OH, and C1-3alkyl optionally substituted with 1-3 F; Ring C is selected from the group consisting of: . c1 is 0, 1, or 2; RYais C1-6 alkyl optionally substituted with 1-3 Rc; each RYbis independently selected from the group consisting of: -F and C1-3 alkyl optionally substituted with 1-3 -F; and yy represents the point of attachment to LA4b. In some embodiments of Formula (I-a) or (I-a1), R2ais H. In some embodiments of Formula (I-a) or (I-a1), Xais N. In some embodiments of Formula (I-a) or (I-a1), R6is halo (e.g., -Cl). In some embodiments of Formula (I-a) or (I-a1), c1 is 0 or 1. In some embodiments of Formula (I-a) or (I-a1), RYais C1-3alkyl optionally substituted with 1-3 -F, and each RYbis -F. In some embodiments of Formula (I-a) or (I-a1), RYais methyl. In some embodiments of Formula (I-a) or (I-a1), Ring C is selected from the group , m4 and m5 are independently 0, 1, or 2; each Ra4and Ra5is independently selected from the group consisting of: -F, CN, C1-3 alkoxy, OH, and C1-3alkyl optionally substituted with 1-3 F; and bb represents the point of attachment to Ring C. For example, the In some embodiments of Formula (I-a) or (I-a1), the LA4a-LA1-LA4bmoiety is , wherein: m4 and m5 are independently 0, 1, or 2; each Ra4is independently selected from the group consisting of: -F, CN, C1-3alkoxy, OH, and C1-3alkyl optionally substituted with 1-3 F; each Ra5is independently C1-3 alkyl optionally substituted with 1-3 F; and bb represents the point of attachment to Ring C. For example, the In some embodiments of Formula (I-a) or (I-a1), the LA4a-LA1-LA4bmoiety is , wherein: m4 and m5 are independently 0, 1, or 2; each Ra4is independently C1-3 alkyl optionally substituted with 1-3 F; each Ra5is independently selected from the group consisting of: -F, CN, C1-3alkoxy, OH, and C1-3 alkyl optionally substituted with 1-3 F; and bb represents the point of attachment to Ring C. For example, the In some embodiments, the compounds of Formula (I) are compounds of Formula (I-b): Formula (I-b) or pharmaceutically acceptable salts thereof, wherein: LA4aand LA4bare independently 4-12 membered nitrogen-containing heterocyclylene optionally substituted with 1-3 Ra; LA1is CH2 or CHRL, RLis selected from the group consisting of: -F, -OH, and C1-3 alkyl optionally substituted with 1-3 Rc(e.g., C1-3alkyl optionally substituted with 1-3 -F); c1 is 1 or 2; RYais C1-6 alkyl optionally substituted with 1-3 Rc; and each RYbis independently selected from the group consisting of: -F and C1-3 alkyl optionally substituted with 1-3 -F. In some embodiments, the compounds of Formula (I-b) are other than Compound Nos. R239 or R240, as depicted in Table R1, or pharmaceutically acceptable salts thereof. In some embodiments of Formula (I-b), one or more of (1)-(3) applies: (1) LA4aand LA4bare independently a 4-6 membered monocyclic nitrogen-containing heterocyclylene optionally substituted with 1-3 Ra; (2) LA4aand LA4bare independently a 4-12 membered nitrogen-containing heterocyclylene substituted with 1-3 Ra; and / or (3) c1 is 2. In some embodiments of Formula (I-b), the moiety is selected from the group consisting of: In some embodiments of Formula (I-b), the LA4a-LA1-LA4bmoiety is , wherein: m4 and m5 are independently 0, 1, or 2; each Ra4and Ra5is independently selected from the group consisting of: -F, CN, C1-3 alkoxy, OH, and C1-3alkyl optionally substituted with 1-3 F; and bb represents the point of attachment t . some embodiments, m5 is 0; and m4 is 0 or 1 (e.g., 0). In some embodiments of Formula (I-b), LA1is CH2. In some embodiments, the compounds of Formula (I) are compounds of Formula (I-c): Formula (I-c) or pharmaceutically acceptable salts thereof, wherein: m4 and m5 are independently 0, 1, or 2; each Ra4and Ra5is independently selected from the group consisting of: -F, CN, C1-3 alkoxy, OH, and C1-3alkyl optionally substituted with 1-3 F; LA1is CH2 or CHRL, wherein RLis selected from the group consisting of: -F, -OH, and C1-3 alkyl optionally substituted with 1-3 Rc(e.g., C1-3alkyl optionally substituted with 1-3 -F); c1 is 0, 1, or 2; RYais C1-6 alkyl optionally substituted with 1-3 Rc; and each RYbis independently selected from the group consisting of: -F and C1-3 alkyl optionally substituted with 1-3 -F. In some embodiments, the compounds of Formula (I-c) are other than Compound Nos. R242, R242a, R242b, R212, or R167, as depicted in Table R1, or pharmaceutically acceptable salts thereof. In some embodiments of Formula (I-c), one or more of (1)-(3) applies: (1) m4 is 1 or 2, wherein each Ra4is independently C1-3 alkyl optionally substituted with 1-3 F; (2) m5 is 1 or 2; and / or (3) c1 is 1 or 2. In some embodiments of Formula (I-c), m4 is 0; and m5 is 0. In some embodiments of Formula (I-c), m4 is 1 or 2, wherein each Ra4is independently C1-3alkyl optionally substituted with 1-3 F; and m5 is 0. In some embodiments of Formula (I-c), LA1is CH2. In some embodiments of Formula (I-c), c1 is 0. In some embodiments of Formula (I-c), c1 is 1 or 2. In some embodiments of Formula (I-c), the moiety is selected from the group consisting of: In some embodiments of Formula (I-b) or (I-c), RYais methyl. In some embodiments of Formula (I-b) or (I-c), each RYbis -F. In some embodiments of Formula (I-b) or (I-c), R5is -NR5ARf. In some embodiments of Formula (I-b) or (I-c), R5is -NH(Me). In some embodiments of Formula (I-b) or (I-c), R2ais H. In some embodiments of Formula (I-b) or (I-c), m3 is 1; and X3is C1-3alkylene. In some embodiments of Formula (I-b) or (I-c), R1is H. In some embodiments of Formula (I-b) or (I-c), –(X3)m3-R1is isopropyl. In some embodiments of Formula (I-b) or (I-c), R6is -Cl. In some embodiments of Formula (I-b) or (I-c), Xais N. In some embodiments of Formula (I-b) or (I-c), R5is -NH(Me); R6is -Cl; and Xais N. In some embodiments, m3 is 1; X3is C1-3 alkylene; and R1is H. In some embodiments of Formula (I-b) or (I-c), X is CH. In some embodiments, the compounds of Formula (I) are selected from the group consisting of the compounds in Table C1, or pharmaceutically acceptable salts thereof. Table C1 Note: In certain compounds of Table C1 or Table R1, one or more stereogenic centers are denoted with the “V3000 enhanced stereochemical notation” (see: support.collaborativedrug.com / hc / en-us / articles / 360020872171-Advanced-Stereochemistry- Registration-Atropisomers-Mixtures-Unknowns-and-Non-Tetrahedral-Chirality, accessed on December 23, 2022 and Accelrys Chemical Representation Guide, Accelrys Software Inc., 2014, each of which is incorporated by reference herein in its entirety). Using this stereochemical notation, certain stereogenic centers are denoted with “abs”, “&x”, or “orx”, wherein x is an integer (e.g., 1 or 2). For avoidance of doubt, the stereochemical notations in Table C1 or Table R1 have the following meaning: (1) When a stereogenic center (e.g., a stereogenic carbon) is depicted with “flat" bonds (i.e., none of the chemical bonds at the stereogenic center is depicted with wedges or dashes) in a structural formula, each of the stereogenic centers can independently adopt the (R)- or (S)- configurations. For example, the structure represents (S)-(1- methylpyrrolidin-2-yl)methanol, (R)-(1-methylpyrrolidin-2-yl)methanol, or a mixture thereof. As another non-limiting example, the structure represents: (3S,5S)-5- methylpiperidine-3-carboxylic acid; (3R,5S)-5-methylpiperidine-3-carboxylic acid; (3S,5R)- 5-methylpiperidine-3-carboxylic acid; (3R,5R)-5-methylpiperidine-3-carboxylic acid; or a mixture thereof. When a stereogenic center or a plurality of stereogenic centers is depicted with wedges and dashes, the following notations are used: (2) When a stereogenic center is denoted with “abs” or when a stereogenic center is not denoted with an enhanced stereochemical notation (e.g., “abs”, “&x”, or “orx”), the stereogenic center has the absolute configuration as depicted by the structural formula. For example, both of the structures and refer to (S)-(1- methylpyrrolidin-2-yl)methanol. (3) When a stereogenic center is denoted with “orx” in a structural formula, the stereogenic center has been resolved but the configuration at the stereogenic center has not been determined. For example, the structure refers to one stereoisomer selected from the group consisting of (S)-(1-methylpyrrolidin-2-yl)methanol and methylpyrrolidin-2-yl)methanol. (4) When two or more stereogenic centers are denoted with “orx” in a structural formula, each of these stereogenic centers has been resolved but the configurations at the stereogenic centers have not been determined. Specifically: a. For any pair of stereogenic centers denoted with “orx” in a structural formula, when the numerical parts in the notation are different (e.g., two stereogenic centers denoted with “or1” and “or2” respectively), each stereogenic center is independently defined according to (3) (vide supra). For example, the structure b. For any pair of stereogenic centers denoted with “orx” in a structural formula, when the numerical part in the notation is identical (e.g., two stereogenic centers each denoted with “or1”), the structural formula refers to one stereoisomer having the relative stereochemistry at these stereogenic centers as depicted in the structural formula, but the absolute configurations of these stereogenic centers have not been determined. For example, the structure refers to one of the two “syn” stereoisomers: . As another example, the structure one of the “anti” stereoisomers: . (5) When two or more stereogenic centers are denoted with “&x” in a structural formula, the structural formula refers to a mixture of stereoisomers that differ in the configuration at the stereogenic centers. Specifically: a. For any pair of stereogenic centers denoted with “&x” in a structural formula, when the numerical parts in the notation are different (e.g., two stereogenic centers denoted with “&1” and “&2” respectively), the structural formula refers to a mixture of stereoisomers at these two stereogenic centers, wherein the configuration at each stereogenic center can vary independently of one refers to a mixture of four . b. For any pair of stereogenic centers denoted with “&x” in a structural formula, when the numerical part in the notation is identical (e.g., two stereogenic centers each denoted with “&1”), the structural formula refers to a mixture of stereoisomers at these two or more stereogenic centers, wherein the relative configurations are as depicted in the structural formula. For example, the structure refers to a mixture of “syn” stereoisomers: a d . As another example, the structure refers to a mixture of “anti” stereoisomers: In some embodiments, the compounds of Formula (I), or pharmaceutically acceptable salts thereof, are selected from the compounds depicted in Table C1 of U.S. Provisional Application Serial No. 63 / 580,215, filed September 1, 2023; Table C1 of U.S. Provisional Application Serial No.63 / 607,012, filed December 6, 2023; Table C1 of U.S. Provisional Application Serial No.63 / 624,171, filed January 23, 2024; and Table C1 of U.S. Provisional Application Serial No.63 / 665,670, filed June 28, 2024; each Table C1 is hereby incorporated by reference in its entirety. In some embodiments, the compounds of Formula (I), or pharmaceutically acceptable salts thereof, are other than the compounds in Table C1 of International Patent Application No. PCT / US / 23 / 67918, filed June 5, 2023, or pharmaceutically acceptable salts thereof, wherein the Table C1 of International Patent Application No. PCT / US / 23 / 67918 is incorporated herein by reference in its entirety. In some embodiments, the compounds of Formula (I), or pharmaceutically acceptable salts thereof, are other than the compounds depicted in Table R1, or pharmaceutically acceptable salts thereof. Table R1

[0002] In some embodiments, the compounds of Formula (I) (e.g., Formula (I-a), (I-a1), (I- b), or (I-c)), or pharmaceutically acceptable salts thereof, reduce cell viability in a cell line expressing a BCL6 protein with an EC50of less than 1 µM (e.g., less than 750 nM, less than 500 nM, or less than 200 nM). In some embodiments, the compounds reduce cell viability in a cell line expressing the BCL6 protein with an EC50 of less than 200 nM (e.g., less than 150 nM, less than 100 nM, less than 10 nM, less than 1 nM). For example, the compounds can reduce cell viability in a cell line expressing the BCL6 protein with an EC50of about 0.1 nM to about 100 nM, about 0.1 nM to about 50 nM, about 1 nM to about 50 nM, about 1 nM to about 20 nM, or about 0.1 nM to about 1 nM. In some embodiments, the compounds of Formula (I) (e.g., Formula (I-a), (I-a1), (I- b), or (I-c)), or pharmaceutically acceptable salts thereof, induce degradation of a BCL6 protein in a cell line expressing the BCL6 protein with a DC50 of less than 1 µM (e.g., less than 750 nM, less than 500 nM, or less than 200 nM). In some embodiments, the compounds of Formula (I) (e.g., Formula (I-a), (I-a1), (I-b), or (I-c)), or pharmaceutically acceptable salts thereof, induce degradation of a BCL6 protein in a cell line expressing the BCL6 protein with a DC50 of less than 200 nM (e.g., less than 150 nM, less than 100 nM, less than 10 nM, less than 1 nM). For example, the compounds can induce degradation of a BCL6 protein in a cell line expressing the BCL6 protein with a DC50 of about 0.1 nM to about 100 nM, about 0.1 nM to about 50 nM, about 1 nM to about 50 nM, about 1 nM to about 20 nM, or about 0.1 nM to about 1 nM. In some embodiments, the compounds of Formula (I) (e.g., Formula (I-a), (I-a1), (I- b), or (I-c)), or pharmaceutically acceptable salts thereof, induce degradation of a BCL6 protein in a cell line expressing the BCL6 protein with a Ymin of less than 70% (e.g., less than 50%, less than 30%, less than 20%, or less than 10%). In some embodiments, the compounds of Formula (I) (e.g., Formula (I-a), (I-a1), (I-b), or (I-c)), or pharmaceutically acceptable salts thereof, induce degradation of a BCL6 protein in a cell line expressing the BCL6 protein with a Yminof less than 50% (e.g., less than 40%, less than 30%, less than 20%, less than 10%, or less than 5%). In some embodiments, the compounds of Formula (I) (e.g., Formula (I-a), (I- a1), (I-b), or (I-c)), or pharmaceutically acceptable salts thereof, induce degradation of a BCL6 protein in a cell line expressing the BCL6 protein with a Yminof less than 30% (e.g., less than 25%, less than 20%, less than 15%, less than 10%, or less than 5%). For example, the compounds can induce degradation of a BCL6 protein in a cell line expressing the BCL6 protein with a Ymin of about 1% to about 70% (e.g., about 5% to about 50% or about 10% to about 30%). Also provided herein is a BCL6 protein non-covalently bound with a compound of Formula (I) (e.g., Formula (I-a), (I-a1), (I-b), or (I-c)), or a pharmaceutically acceptable salt thereof. Also provided herein is a ternary complex comprising a BCL6 protein, a compound of Formula (I) (e.g., Formula (I-a), (I-a1), (I-b), or (I-c)), or a pharmaceutically acceptable salt thereof, and a CRBN protein or a portion thereof. Chemical definitions The term “halo” refers to fluoro (F), chloro (Cl), bromo (Br), or iodo (I). The term “oxo” refers to a divalent doubly bonded oxygen atom (i.e., “=O”). As used herein, oxo groups are attached to carbon atoms to form carbonyls. The term “alkyl” refers to a saturated acyclic hydrocarbon radical that may be a straight chain or branched chain, containing the indicated number of carbon atoms. For example, C1-10indicates that the group may have from 1 to 10 (inclusive) carbon atoms in it. Alkyl groups can either be unsubstituted or substituted with one or more substituents. Non-limiting examples include methyl, ethyl, iso-propyl, tert-butyl, n-hexyl. The term “saturated” as used in this context means only single bonds present between constituent carbon atoms and other available valences occupied by hydrogen and / or other substituents as defined herein. The term “haloalkyl” refers to an alkyl, in which one or more hydrogen atoms is / are replaced with an independently selected halo (e.g., -CF3, -CHF2, or -CH2F). The term “alkoxy” refers to an -O-alkyl radical (e.g., -OCH3). The term “alkylene” refers to a divalent alkyl (e.g., -CH2-). Similarly, terms such as “cycloalkylene” and “heterocyclylene” refer to divalent cycloalkyl and heterocyclyl respectively. For avoidance of doubt, in “cycloalkylene” and “heterocyclylene”, the two radicals can be on the same ring carbon atom (e.g., a geminal diradical such ) or on different ring atoms (e.g., ring carbon and / or nitrogen atoms (e.g., vicinal ring carbon and / or nitrogen atoms) The term “alkenyl” refers to an acyclic hydrocarbon chain that may be a straight chain or branched chain having one or more carbon-carbon double bonds. The alkenyl moiety contains the indicated number of carbon atoms. For example, C2-6indicates that the group may have from 2 to 6 (inclusive) carbon atoms in it. Alkenyl groups can either be unsubstituted or substituted with one or more substituents. The term “alkynyl” refers to an acyclic hydrocarbon chain that may be a straight chain or branched chain having one or more carbon-carbon triple bonds. The alkynyl moiety contains the indicated number of carbon atoms. For example, C2-6 indicates that the group may have from 2 to 6 (inclusive) carbon atoms in it. Alkynyl groups can either be unsubstituted or substituted with one or more substituents. The term “aryl” refers to a 6-20 carbon mono-, bi-, tri- or polycyclic group wherein at least one ring in the system is aromatic (e.g., 6-carbon monocyclic, 10-carbon bicyclic, or 14- carbon tricyclic aromatic ring system); and wherein 0, 1, 2, 3, or 4 atoms of each ring may be substituted by a substituent. Examples of aryl groups include phenyl, naphthyl, tetrahydronaphthyl, and the like. The term “cycloalkyl” as used herein refers to mono-, bi-, tri-, or polycyclic saturated or partially unsaturated hydrocarbon groups having, e.g., 3 to 20 ring carbons, preferably 3 to 15 ring carbons, and more preferably 3 to 12 ring carbons or 3-10 ring carbons or 3-6 ring carbons, wherein the cycloalkyl group may be optionally substituted. The term “saturated” as used in this context means only single bonds present between constituent carbon atoms. Examples of saturated cycloalkyl groups include, without limitation, cyclopropyl, cyclobutyl, cyclopentyl, cyclohexyl, cycloheptyl, and cyclooctyl. Partially unsaturated cycloalkyl may have any degree of unsaturation provided that one or more double bonds is present in the cycloalkyl, none of the rings in the ring system are aromatic, and the partially unsaturated cycloalkyl group is not fully saturated overall. Examples of partially unsaturated cycloalkyl include, without limitation, cyclopentenyl, cyclohexenyl, cycloheptenyl, and cyclooctenyl. Cycloalkyl may include multiple fused and / or bridged rings. Non-limiting examples of fused / bridged cycloalkyl includes: bicyclo[1.1.0]butyl, bicyclo[2.1.0]pentyl, bicyclo[1.1.1]pentyl, bicyclo[3.1.0]hexyl, bicyclo[2.1.1]hexyl, bicyclo[3.2.0]heptyl, bicyclo[4.1.0]heptyl, bicyclo[2.2.1]heptyl, bicyclo[3.1.1]heptyl, bicyclo[4.2.0]octyl, bicyclo[3.2.1]octyl, bicyclo[2.2.2]octyl, and the like. Cycloalkyl also includes spirocyclic rings (e.g., spirocyclic bicycle wherein two rings are connected through just one atom). Non-limiting examples of spirocyclic cycloalkyls include spiro[2.2]pentyl, spiro[2.5]octyl, spiro[3.5]nonyl, spiro[3.5]nonyl, spiro[3.5]nonyl, spiro[4.4]nonyl, spiro[2.6]nonyl, spiro[4.5]decyl, spiro[3.6]decyl, spiro[5.5]undecyl, and the like. The term “heteroaryl”, as used herein, means a mono-, bi-, tri- or polycyclic group having 5 to 20 ring atoms, alternatively 5, 6, 9, 10, or 15 ring atoms; wherein at least one ring in the system contains one or more heteroatoms independently selected from the group consisting of N, O, and S (inclusive of oxidized forms such as: and at least one ring in the system is aromatic (but does not have to be a ring which contains a heteroatom, e.g. tetrahydroisoquinolinyl, e.g., tetrahydroquinolinyl). In some embodiments, heteroaryl groups contain 1-4 (e.g., 1, 2, or 3) ring heteroatoms each independently selected from the group consisting of N, O, and S (inclusive of oxidized forms such as: Heteroaryl groups can either be unsubstituted or substituted with one or more substituents. Examples of heteroaryl include thienyl, pyridinyl, furyl, oxazolyl, oxadiazolyl, pyrrolyl, imidazolyl, triazolyl, thiodiazolyl, pyrazolyl, isoxazolyl, thiadiazolyl, pyranyl, pyrazinyl, pyrimidinyl, pyridazinyl, triazinyl, thiazolyl benzothienyl, benzoxadiazolyl, benzofuranyl, benzimidazolyl, benzotriazolyl, cinnolinyl, indazolyl, indolyl, isoquinolinyl, isothiazolyl, naphthyridinyl, purinyl, thienopyridinyl, pyrido[2,3-d]pyrimidinyl, pyrrolo[2,3-b]pyridinyl, quinazolinyl, quinolinyl, thieno[2,3-c]pyridinyl, pyrazolo[3,4-b]pyridinyl, pyrazolo[3,4- c]pyridinyl, pyrazolo[4,3-c]pyridinyl, pyrazolo[4,3-b]pyridinyl, tetrazolyl, chromanyl, 2,3- dihydrobenzo[b][1,4]dioxinyl, benzo[d][1,3]dioxolyl, 2,3-dihydrobenzofuranyl, tetrahydroquinolinyl, 2,3-dihydrobenzo[b][1,4]oxathiinyl, isoindolinyl, and others. In some embodiments, the heteroaryl is selected from thienyl, pyridinyl, furyl, pyrazolyl, imidazolyl, isoindolinyl, pyranyl, pyrazinyl, and pyrimidinyl. For purposes of clarification, heteroaryl also includes aromatic lactams, aromatic cyclic ureas, or vinylogous analogs thereof, in which each ring nitrogen adjacent to a carbonyl is tertiary (i.e., all three valences are occupied by non- hydrogen substituents), such as one or more of pyridone (e.g., , , , ), wherein each ring nitrogen adjacent to a carbonyl is tertiary (i.e., the oxo group (i.e., “=O”) herein is a constituent part of the heteroaryl ring). The term “heterocyclyl” refers to a mono-, bi-, tri-, or polycyclic saturated or partially unsaturated ring system with 3-15 ring atoms (e.g., 5-8 membered monocyclic, 8-12 membered bicyclic, or 11-15 membered tricyclic ring system) having 1-3 heteroatoms if monocyclic, 1-6 heteroatoms if bicyclic, or 1-9 heteroatoms if tricyclic or polycyclic, the heteroatoms selected from O, N, and S (inclusive of oxidized forms such as: ) (e.g., carbon atoms and 1-3, 1-6, or 1-9 heteroatoms of N, O, S, or P if monocyclic, bicyclic, or tricyclic, respectively), wherein 0, 1, 2 or 3 atoms of each ring may be substituted by a substituent. The term “saturated” as used in this context means only single bonds present between constituent ring atoms and other available valences occupied by hydrogen and / or other substituents as defined herein. Examples of saturated heterocyclyl groups include piperazinyl, pyrrolidinyl, dioxanyl, morpholinyl, tetrahydrofuranyl, and the like. Partially unsaturated heterocyclyl groups may have any degree of unsaturation provided that one or more double bonds is present in the heterocyclyl, none of the rings in the ring system are aromatic, and the partially unsaturated heterocyclyl group is not fully saturated overall. Examples of partially unsaturated heterocyclyl groups include, without limitation, tetrahydropyridyl, dihydropyrazinyl, dihydropyridyl, dihydropyrrolyl, dihydrofuranyl, dihydrothiophenyl. Heterocyclyl may include multiple fused and bridged rings. Non-limiting examples of fused / bridged heteorocyclyl includes: 2-azabicyclo[1.1.0]butyl, 2-azabicyclo[2.1.0]pentyl, 2- azabicyclo[1.1.1]pentyl, 3-azabicyclo[3.1.0]hexyl, 5-azabicyclo[2.1.1]hexyl, 3- azabicyclo[3.2.0]heptyl, octahydrocyclopenta[c]pyrrolyl, 3-azabicyclo[4.1.0]heptyl, 7- azabicyclo[2.2.1]heptyl, 6-azabicyclo[3.1.1]heptyl, 7-azabicyclo[4.2.0]octyl, 2- azabicyclo[2.2.2]octyl, 3-azabicyclo[3.2.1]octyl, 2-oxabicyclo[1.1.0]butyl, 2- oxabicyclo[2.1.0]pentyl, 2-oxabicyclo[1.1.1]pentyl, 3-oxabicyclo[3.1.0]hexyl, 5- oxabicyclo[2.1.1]hexyl, 3-oxabicyclo[3.2.0]heptyl, 3-oxabicyclo[4.1.0]heptyl, 7- oxabicyclo[2.2.1]heptyl, 6-oxabicyclo[3.1.1]heptyl, 7-oxabicyclo[4.2.0]octyl, 2- oxabicyclo[2.2.2]octyl, 3-oxabicyclo[3.2.1]octyl, and the like. Heterocyclyl also includes spirocyclic rings (e.g., spirocyclic bicycle wherein two rings are connected through just one atom). Non-limiting examples of spirocyclic heterocyclyls include 2-azaspiro[2.2]pentyl, 4- azaspiro[2.5]octyl, 1-azaspiro[3.5]nonyl, 2-azaspiro[3.5]nonyl, 7-azaspiro[3.5]nonyl, 2- azaspiro[4.4]nonyl, 6-azaspiro[2.6]nonyl, 1,7-diazaspiro[4.5]decyl, 7-azaspiro[4.5]decyl 2,5- diazaspiro[3.6]decyl, 3-azaspiro[5.5]undecyl, 2-oxaspiro[2.2]pentyl, 4-oxaspiro[2.5]octyl, 1- oxaspiro[3.5]nonyl, 2-oxaspiro[3.5]nonyl, 7-oxaspiro[3.5]nonyl, 2-oxaspiro[4.4]nonyl, 6- oxaspiro[2.6]nonyl, 1,7-dioxaspiro[4.5]decyl, 2,5-dioxaspiro[3.6]decyl, 1- oxaspiro[5.5]undecyl, 3-oxaspiro[5.5]undecyl, 3-oxa-9-azaspiro[5.5]undecyl and the like. A nitrogen-containing heterocyclyl as used herein refers to a heterocyclyl having 1-2 ring nitrogen atoms and 0-2 additional ring heteroatoms selected from the group consisting of O and S (inclusive of oxidized such as: or . The nitrogen-containing heterocyclyl can be monocyclic, bicyclic, or polycyclic as defined elsewhere herein. Examples of monocyclic nitrogen-containing heterocyclyl include azetidinyl, pyrrolidinyl, piperidinyl, piperazinyl, morpholinyl, and the like. Examples of bicyclic nitrogen-containing heterocyclyl include 7-azaspiro[3.5]nonyl, 1,7-diazaspiro[4.5]decyl, 3-oxa-7,9-diazabicyclo[3.3.1]nonanyl, 2,6-diazaspiro[3.3]heptanyl, and the like. As used herein, when a ring is described as being “partially unsaturated”, it means the ring has one or more additional degrees of unsaturation (in addition to the degree of unsaturation attributed to the ring itself; e.g., one or more double or triple bonds between constituent ring atoms), provided that the ring is not aromatic. Examples of such rings include: cyclopentene, cyclohexene, cycloheptene, dihydropyridine, tetrahydropyridine, dihydropyrrole, dihydrofuran, dihydrothiophene, and the like. For the avoidance of doubt, and unless otherwise specified, for rings and cyclic groups (e.g., aryl, heteroaryl, heterocyclyl, heterocycloalkenyl, cycloalkenyl, cycloalkyl, and the like described herein) containing a sufficient number of ring atoms to form bicyclic or higher order ring systems (e.g., tricyclic, polycyclic ring systems), it is understood that such rings and cyclic groups encompass those having fused rings, including those in which the points of fusion are located (i) on adjacent ring atoms (e.g., [x.x.0] ring systems, in which 0 represents a zero atom bridge (e.g. a single ring atom (spiro-fused ring systems) (e.g., or (iii) a contiguous array of ring atoms (bridged ring systems having all bridge lengths In addition, atoms making up the compounds of the present embodiments are intended to include all isotopic forms of such atoms. Isotopes, as used herein, include those atoms having the same atomic number but different mass numbers. By way of general example and without limitation, isotopes of hydrogen include tritium and deuterium, and isotopes of carbon include 13C and14C. In addition, the compounds generically or specifically disclosed herein are intended to include all tautomeric forms. Thus, by way of example, a compound containing the moiety: encompasses the tautomeric form containing the moiety: . Similarly, a pyridinyl or pyrimidinyl moiety that is described to be optionally substituted with hydroxyl encompasses pyridone or pyrimidone tautomeric forms. The compounds provided herein may encompass various stereochemical forms. The compounds also encompass diastereomers as well as optical isomers, e.g., mixtures of enantiomers including racemic mixtures, as well as individual enantiomers and diastereomers, which arise as a consequence of structural asymmetry in certain compounds. Unless otherwise indicated, when a disclosed compound is named or depicted by a structure without specifying the stereochemistry and has one or more chiral centers, it is understood to represent all possible stereoisomers of the compound. Methods of Treatment Indications Provided herein are methods for inducing degradation of a BCL6 protein. For example, provided herein are compounds capable of inducing degradation of a BCL6 protein useful for treating or preventing cancers. Exemplary compounds that bind to BCL6 are described in, e.g., Cerchietti, Leandro C., et al. Cancer Cell 17.4 (2010): 400-411, doi: 10.1016 / j.ccr.2009.12.050; Cardenas, Mariano G., et al. The Journal of Clinical Investigation 126(9) (2016): 3351-3362, doi: 10.1172 / JCI85795; Kerres, Nina, et al., Cell Reports 20.12 (2017): 2860-2875, doi: 10.1016 / j.celrep.2017.08.081; Yasui, Takeshi, et al., Bioorganic & Medicinal Chemistry 25.17 (2017): 4876-4886, doi: 10.1016 / j.bmc.2017.07.037; Kamada, Yusuke, et al., Journal of Medicinal Chemistry 60.10 (2017): 4358-4368, doi: 10.1021 / acs.jmedchem.7b00313; McCoull, William, et al., ACS Chemical Biology 13.11 (2018): 3131-3141, doi: 10.1021 / acschembio.8b00698; Guo, Weikai, et al. Journal of Medicinal Chemistry 63.2 (2020): 676-695, doi: 10.1021 / acs.jmedchem.9b01618; Teng, Mingxing, et al., ACS Medicinal Chemistry Letters 11.6 (2020): 1269-1273, doi: 10.1021 / acsmedchemlett.0c00111; Pearce, Andrew C., et al., Journal of Biological Chemistry 297.2 (2021): 100928, doi: 10.1016 / j.jbc.2021.100928; Ding, Shu, Yu Rao, and Qianjin Lu, Cellular & Molecular Immunology (2022): 1-3, doi: 10.1038 / s41423-022-00882-1; Xing, Y. et al., Cancer Letters (2022), doi: 10.1016 / j.canlet.2021.12.035; Huckvale, R. et al., Journal of Medicinal Chemistry (2022), doi: 10.1021 / acs.jmedchem.1c02175; Davis, O. et al., Journal of Medicinal Chemistry (2022), doi: 10.1021 / acs.jmedchem.1c02174; International Publication Nos. WO 2008 / 066887; WO 2010 / 008436; WO 2014 / 204859; WO 2018 / 215798; WO 2018 / 215801; WO 2018 / 219281; WO 2019 / 119138; WO 2019 / 119144; WO 2019 / 119145; WO 2019 / 153080; WO 2019 / 197842; WO 2020 / 104820; WO 2021 / 074620; WO 2021 / 077010; WO 2022 / 221673; WO 2023 / 212147; and WO 2023 / 114460. The term “compound(s) provided herein” refers to compound(s) of Formula (I) (e.g., Formula (I-a), (I-a1), (I-b), or (I-c)) as disclosed herein. Potency of degradation by a compound provided herein, or a pharmaceutically acceptable salt thereof, can be determined by DC50value. As used herein, DC50refers to the concentration of the compound provided herein, or a pharmaceutically acceptable salt thereof, that results in a 50% decrease in the concentration of a protein (e.g., BCL6 protein) in a cell compared to the concentration of the protein before the cell is contacted with the compound provided herein, or a pharmaceutically acceptable salt thereof, or compared to the concentration of the protein in a cell not contacted with the compound provided herein, or a pharmaceutically acceptable salt thereof. A compound with a lower DC50 value, as determined under substantially similar conditions, is a more potent inducer of degradation relative to a compound with a higher DC50 value. In some embodiments, a DC50 value can be determined (e.g., using HiBiT detection) in vitro or in vivo (e.g., in tumor cells expressing a BCL6 protein (e.g., cell lines such as A3 / KAW, A4 / FUK, DB, DOHH2, Farage, HT, Karpas 422, KML1, MHHPREB1, NUDHL1, OCI-Ly1, OCI-Ly3, OCI-Ly7, OCI-Ly18, OCI-Ly19, Pfeiffer, RI1, RL, SU-DHL-4, SU-DHL-5, SU-DHL-6, SU-DHL-8, SU-DHL-10, VAL, or WSU-DLCL2; see also those disclosed in, e.g., Cardenas, Mariano G., et al. Clinical Cancer Research 23.4 (2017): 885-893, doi: 10.1158 / 1078-0432.CCR-16-2071 and International Publication Nos. WO 2021 / 080950, WO 2021 / 077010, and WO 2022 / 221673)). In some embodiments, a cell line that is not dependent on BCL6 and / or that does not have significant expression of BCL6 can be used as a control (e.g., Toledo, H929, MM.1S, or OPM2). Potency of degradation by a compound provided herein, or a pharmaceutically acceptable salt thereof, can be determined by EC50 value. As used herein, EC50 refers to the concentration of the compound provided herein, or a pharmaceutically acceptable salt thereof, that results in a 50% decrease in the concentration of a protein (e.g., BCL6 protein) relative to the trough concentration of the protein in a cell, when compared to the concentration of the protein before the cell is contacted with the compound provided herein, or a pharmaceutically acceptable salt thereof, or compared to the concentration of the protein in a cell not contacted with the compound provided herein, or a pharmaceutically acceptable salt thereof. A compound with a lower EC50 value, as determined under substantially similar conditions, is a more potent inducer of degradation relative to a compound with a higher EC50value. In some embodiments, an EC50value can be determined (e.g., using HiBiT detection) in vitro or in vivo (e.g., in tumor cells expressing a BCL6 protein (e.g., cell lines such as A3 / KAW, A4 / FUK, DB, DOHH2, Farage, HT, Karpas 422, KML1, MHHPREB1, NUDHL1, OCI-Ly1, OCI-Ly3, OCI-Ly7, OCI-Ly18, OCI-Ly19, Pfeiffer, RI1, RL, SU-DHL-4, SU-DHL-5, SU-DHL-6, SU-DHL-8, SU-DHL-10, VAL, or WSU-DLCL2; see also those disclosed in, e.g., Cardenas, Mariano G., et al. Clinical Cancer Research 23.4 (2017): 885-893, doi: 10.1158 / 1078-0432.CCR-16-2071 and International Publication Nos. WO 2021 / 080950,WO 2021 / 077010, and WO 2022 / 221673)). In some embodiments, a cell line that is not dependent on BCL6 and / or that does not have significant expression of BCL6 can be used as a control (e.g., Toledo, H929, MM.1S, or OPM2). Potency of degradation by a compound provided herein, or a pharmaceutically acceptable salt thereof, can be determined by a Ymin value. As used herein, Ymin refers to the ratio of trough concentration of a protein (e.g., BCL6 protein) in a cell compared to the concentration of the protein before the cell is contacted with the compound provided herein, or a pharmaceutically acceptable salt thereof, or compared to the concentration of the protein in a cell not contacted with the compound provided herein, or a pharmaceutically acceptable salt thereof, expressed as a percentage. As used herein, Dmaxis 1-Ymin. Ymincan be measured by a HiBiT assay (e.g., as described in Example B1). A compound with a lower Ymin value, as determined under substantially similar conditions, is a more potent inducer of degradation relative to a compound with a higher Yminvalue. In some embodiments, a Yminvalue can determined (e.g., using HiBiT detection), in vitro or in vivo (e.g., in tumor cells expressing a BCL6 protein (e.g., cell lines such as A3 / KAW, A4 / FUK, DB, DOHH2, Farage, HT, Karpas 422, KML1, MHHPREB1, NUDHL1, OCI-Ly1, OCI-Ly3, OCI-Ly7, OCI-Ly18, OCI-Ly19, Pfeiffer, RI1, RL, SU-DHL-4, SU-DHL-5, SU-DHL-6, SU-DHL-8, SU-DHL-10, VAL, or WSU-DLCL2; see also those disclosed in, e.g., Cardenas, Mariano G., et al. Clinical Cancer Research 23.4 (2017): 885-893, doi: 10.1158 / 1078-0432.CCR-16-2071 and International Publication Nos. WO 2021 / 080950, WO 2021 / 077010, and WO 2022 / 221673)). In some embodiments, a cell line that is not dependent on BCL6 and / or that does not have significant expression of BCL6 can be used as a control (e.g., Toledo, H929, MM.1S, or OPM2). In some embodiments, a compound provided herein, or a pharmaceutically acceptable salt thereof, exhibits a Yminof less than 70% (e.g., less than 50% or less than 30%) in a HiBiT based degradation assay (e.g., an assay as described in Example B1). In some embodiments, a compound provided herein, or a pharmaceutically acceptable salt thereof, exhibits a Ymin of less than 50% (e.g., less than 30%) in a HiBiT based degradation assay. In some embodiments, a compound provided herein, or a pharmaceutically acceptable salt thereof, exhibits a Yminof less than 30% in a HiBiT based degradation assay. In some embodiments, a compound provided herein, or a pharmaceutically acceptable salt thereof, exhibits a Yminof less than 70% (e.g., less than 50% or less than 30%) in the assay described in Example B1. In some embodiments, a compound provided herein, or a pharmaceutically acceptable salt thereof, exhibits a Ymin of less than 50% (e.g., less than 30%) in the assay described in Example B1. In some embodiments, a compound provided herein, or a pharmaceutically acceptable salt thereof, exhibits a Ymin of less than 30% in the assay described in Example B1. In some embodiments, a compound provided herein, or a pharmaceutically acceptable salt thereof, exhibits a Yminof about 0% to about 70% (e.g., about 0% to about 50%, about 30% to about 50%, or about 0% to about 30%) in a HiBiT based degradation assay (e.g., an assay as described in Example B1). In some embodiments, a compound provided herein, or a pharmaceutically acceptable salt thereof, exhibits a Yminof about 0% to about 50% (e.g., about 30% to about 50% or about 0% to about 30%) in a HiBiT based degradation assay. In some embodiments, a compound provided herein, or a pharmaceutically acceptable salt thereof, exhibits a Yminof about 0% to about 30% in a HiBiT based degradation assay. In some embodiments, a compound provided herein, or a pharmaceutically acceptable salt thereof, exhibits a Ymin of about 0% to about 70% (e.g., about 0% to about 50%, about 30% to about 50%, or about 0% to about 30%) in the assay described in Example B1. In some embodiments, a compound provided herein, or a pharmaceutically acceptable salt thereof, exhibits a Ymin of about 0% to about 50% (e.g., about 30% to about 50% or about 0% to about 30%) in the assay described in Example B1. In some embodiments, a compound provided herein, or a pharmaceutically acceptable salt thereof, exhibits a Yminof about 0% to about 30% in the assay described in Example B1. The effect of protein degradation typically increases over time, though the appearance of degradation (e.g., as expressed by the percentage degradation compared to a control, or the parameters Ymin, DC50, and / or Dmax) is affected by the resynthesis rate of the protein. Accordingly, degradation can be examined after a specified period of time, such as 6 hours, 12 hours, 18 hours, 1 day, 2 days, 3 days, 5 days, 10 days, or more. For example, degradation can be expressed as the percent degradation after 24 hours. Exemplary assays for validating the degradation-inducing mechanism of a compound as provided herein are known in the art and are described, for example, in Wu, et al. Nature Structural & Molecular Biology 27.7 (2020): 605-614, doi: 10.1038 / s41594-020-0438-0. Degradation assays can be used to quantify both on- and off-target degradation- inducing effects of compounds, such as those compounds provided herein. Exemplary assays include quantitative immunoblotting, other immunoassays (e.g., MesoScale Discovery (MSD) immunoassays), homogenous time resolved florescence (HTRF), and HiBiT. In some embodiments, cells can be contacted with a compound provided herein, or a pharmaceutically acceptable salt thereof, incubated, and then the lysate can be prepared for gel electrophoresis (e.g., SDS-PAGE), followed by immunoblotting and quantification compared to a control (e.g., a DMSO-treated control). As another example, a cell line can be engineered to express a HiBiT- tagged BCL6 protein, and the amount of fluorescence observed when the complementary LgBiT peptide is added can be compared between cells treated with a compound provided herein, or a pharmaceutically acceptable salt thereof, and a control (e.g., a DMSO-treated control). See, for instance, Example B1. In some embodiments, off-target degradation inducing effects can be assessed for the proteins Eukaryotic peptide chain release factor GTP- binding subunit ERF3A (GSPT1), Ikaros (IKZF1), Helios (IKZF2), Aiolos (IKZF3), and / or casein kinase I isoform alpha (CK1α). See also, e.g., International Publication Nos. WO 2018 / 215798; WO 2018 / 215801; WO 2020 / 104820; McCoull, William, et al., ACS Chemical Biology 13.11 (2018): 3131-3141, doi: 10.1021 / acschembio.8b00698; Bellenie, Benjamin R., et al., Journal of Medicinal Chemistry 63.8 (2020): 4047-4068, doi: 10.1021 / acs.jmedchem.9b02076; Lloyd, Matthew G., et al., Journal of Medicinal Chemistry 64.23 (2021): 17079-17097, doi: 10.1021 / acs.jmedchem.1c00946. Binding affinity of a compound provided herein, or a pharmaceutically acceptable salt thereof, to BCL6 can be determined by, for example, a binding IC50 or Ki value (e.g., using a competition assay), or by a KD value (e.g., using a biophysical assay). A compound with a lower binding IC50value, as determined under substantially similar conditions, is a more potent binder relative to a compound with a higher binding IC50 value. A compound with a lower binding Ki value, as determined under substantially similar conditions, is a more potent binder relative to a compound with a higher binding Kivalue. Similarly, a compound with a lower KD value, as determined under substantially similar conditions, is a more potent binder relative to a compound with a higher KD value. A KD value can be determined by surface plasmon resonance (SPR) or biolayer interferometry; see, e.g., Guo, Weikai, et al., Journal of Medicinal Chemistry 63.2 (2020): 676-695, doi: 10.1021 / acs.jmedchem.9b01618; Lloyd, Matthew G., et al., Journal of Medicinal Chemistry 64.23 (2021): 17079-17097, doi: 10.1021 / acs.jmedchem.1c00946, and International Publication Nos. WO 2019 / 153080; WO 2019 / 119144; and WO 2019 / 119145. The ability of a compound provided herein, or a pharmaceutically acceptable salt thereof, to inhibit BCL6 can be determined using an IC50 value. A compound with a lower IC50value, as determined under substantially similar conditions, is a more potent inhibitor relative to a compound with a higher IC50value. For example, an IC50value can be calculated using a FRET (e.g., Homogeneous Time Resolved Fluorescence (HTRF)) assay, where a tagged (e.g., His-tagged) BCL6 protein and tagged (e.g., fluorophore-tagged (e.g., Alexa- Fluor633)) corepressor peptide (e.g., BCOR) are incubated in the presence of compounds provided herein, or pharmaceutically acceptable salts thereof, and subsequently, the FRET ratio (relative to appropriate controls) can be measured using an appropriate FRET pair (e.g., with an antibody that recognizes the tagged BCL6 protein (e.g., anti-His-Terbium cryptate)). See, e.g., International Publication Nos. WO 2018 / 108704; WO 2018 / 215798; WO 2019 / 197842; WO 2020 / 104820; WO 2021 / 074620. As another example, an IC50 value can be calculated using an enzyme-linked immunosorbent assay (ELISA) using a tagged (e.g., biotinylated) corepressor peptide (e.g., BCOR) immobilized on a substrate and a tagged (e.g., FLAG-tagged) BCL6 (e.g., a domain, such as the BTB domain, thereof), where compounds provided herein, or pharmaceutically acceptable salts thereof, can be used to prevent the interaction between the corepressor peptide and BCL6, and the interaction between the corepressor peptide and BCL6 can be measured using an antibody to the BCL6 construct (e.g., anti-FLAG antibody). See, e.g., Kamada, Yusuke, et al., Journal of Medicinal Chemistry 60.10 (2017): 4358-4368, doi: 10.1021 / acs.jmedchem.7b00313. As yet another example, an IC50value can be calculated using a florescence polarization assay with a fluorescently-tagged corepressor peptide (e.g., SMRT) where compounds provided herein, or pharmaceutically acceptable salts thereof, can be used to prevent the interaction between the corepressor peptide and BCL6. See, e.g., International Publication No. WO 2019 / 119144. As another example, a cellular IC50value can be calculated using a BRET (Bioluminescence Resonance Energy Transfer) assay, where vectors encoding BCL6 and a corepressor peptide (e.g., SMRT), complementarily fused with NanoLuc or HaloTag, can be inserted into cells. The cells can be treated with compounds provided herein, or pharmaceutically acceptable salts thereof, to determine the effect of the compounds on inhibiting the BCL6-corepressor interaction. See, e.g., International Publication Nos. WO 2018 / 215798 and WO 2019 / 197842. In another example, an IC50value for the inhibition of BCL6 repressor function can be calculated using a luciferase assay, where cells are engineered to express luciferase under the control of one or more BCL6 repressor sites, and the cells can be incubated with compounds provided herein, or pharmaceutically acceptable salts thereof, to determine the effect of the compounds on the function of the BCL6 repressor. See, e.g., International Publication Nos. WO 2019 / 119144; WO 2019 / 119145; WO 2019 / 153080. Another exemplary way of evaluating the effect of a compound provided herein, or a pharmaceutically acceptable salt thereof, is to measure the induction (e.g., fold induction) of genes that are typically repressed by BCL6 (e.g., p53, ATR, CXCR3, CD69, and CDKN1A) using a method such as RT-PCR. See, e.g., Guo, Weikai, et al., Journal of Medicinal Chemistry 63.2 (2020): 676-695, doi: 10.1021 / acs.jmedchem.9b01618. An exemplary assay for determining the potency of a compound provided herein, or a pharmaceutically acceptable salt thereof, includes measuring the effect of the compound provided herein, or a pharmaceutically acceptable salt thereof, on cell proliferation and / or viability. Cell proliferation assays can be performed in a number of formats, including 2D and 3D. Similarly, a cell proliferation assay can be performed with any appropriate cell line, including, for example, A3 / KAW, A4 / FUK, DB, DOHH2, Farage, HT, Karpas 422, KML1, MHHPREB1, NUDHL1, OCI-Ly1, OCI-Ly3, OCI-Ly7, OCI-Ly18, OCI-Ly19, Pfeiffer, RI1, RL, SU-DHL-4, SU-DHL-5, SU-DHL-6, SU-DHL-8, SU-DHL-10, VAL, or WSU-DLCL2. In some embodiments, a cell line that is not dependent on BCL6 and / or that does not have significant expression of BCL6 can be used as a control (e.g., Toledo, H929, MM.1S, or OPM2). As an illustrative example, a 3D cell proliferation assay can include growing cells in a 3D medium, contacting the cells with a compound provided herein, or a pharmaceutically acceptable salt thereof, measuring the cellular proliferation using an appropriate reagent (e.g., CELLTITER-GLO® 3D), and then comparing the signal from the experiment with the compound provided herein, or a pharmaceutically acceptable salt thereof, to the signal from a control experiment (e.g., lacking the compound provided herein, or a pharmaceutically acceptable salt thereof). As another illustrative example, a 2D cell proliferation assay can include plating cells onto a growth surface, optionally letting the cells grow for a period of time, contacting the cells with a compound provided herein, or a pharmaceutically acceptable salt thereof, measuring the cellular proliferation using an appropriate reagent (e.g., CELLTITER-GLO®), and then comparing the signal from an experiment with a compound provided herein, or a pharmaceutically acceptable salt thereof, to the signal from a control experiment (e.g., lacking a compound provided herein, or a pharmaceutically acceptable salt thereof). Additional cell viability assays include MTT assays, which are colorimetric assays based on the reduction of the tetrazolium dye MTT (3-(4,5-dimethylthiazol-2-yl)-2,5- diphenyltetrazolium bromide) to the insoluble purple formazan, and other similar assays based on related tetrazolium salts, ATPlite assays, and other methods are known in the art. See, for instance, Example B2. See also, e.g., Guo, Weikai, et al., Journal of Medicinal Chemistry 63.2 (2020): 676-695, doi: 10.1021 / acs.jmedchem.9b01618; McCoull, William, et al. ACS Chemical Biology 13.11 (2018): 3131-3141, doi: 10.1021 / acschembio.8b00698; Lloyd, Matthew G., et al. Journal of Medicinal Chemistry 64.23 (2021): 17079-17097, doi: 10.1021 / acs.jmedchem.1c00946; Bellenie, Benjamin R., et al. Journal of Medicinal Chemistry 63.8 (2020): 4047-4068, doi: 10.1021 / acs.jmedchem.9b02076; and International Publication Nos. WO 2018 / 215798; WO 2018 / 215801; WO 2018 / 219281; WO 2019 / 119145; WO 2019 / 153080; and WO 2020 / 104820. A cell viability assay can be used to measure the effect of a compound provided herein, or a pharmaceutically acceptable salt thereof, on cell death. For example, cells expressing BCL6 protein (e.g., A3 / KAW, A4 / FUK, DB, DOHH2, Farage, HT, Karpas 422, KML1, MHHPREB1, NUDHL1, OCI-Ly1, OCI-Ly3, OCI-Ly7, OCI-Ly18, OCI-Ly19, Pfeiffer, RI1, RL, SU-DHL-4, SU-DHL-5, SU-DHL-6, SU-DHL-8, SU-DHL-10, VAL, or WSU-DLCL2 cells) can be incubated with various concentrations of a compound provided herein, or a pharmaceutically acceptable salt thereof, and then exposed to a detection reagent (e.g., using a CELLTITER-GLO® Cell Viability Assay kit) to determine cell viability. In some embodiments, the effect on cell viability can be compared to a cell line that is not dependent on BCL6 and / or that does not have significant expression of BCL6 (e.g., Toledo, H929, MM.1S, or OPM2). A cell viability assay can be used to measure the effect of a compound provided herein, or a pharmaceutically acceptable salt thereof, on cell death in combination with an additional therapeutic agent. For example, cells expressing BCL6 protein (e.g., A3 / KAW, A4 / FUK, DB, DOHH2, Farage, HT, Karpas 422, KML1, MHHPREB1, NUDHL1, OCI-Ly1, OCI-Ly3, OCI- Ly7, OCI-Ly18, OCI-Ly19, Pfeiffer, RI1, RL, SU-DHL-4, SU-DHL-5, SU-DHL-6, SU-DHL- 8, SU-DHL-10, VAL, or WSU-DLCL2 cells) can be incubated (e.g., for 72 hours or for 120 hours) in a 7x7 dose matrix at various concentrations of a compound provided herein, or a pharmaceutically acceptable salt thereof, and an additional therapeutic agent (e.g., any of the additional therapeutic agents described herein) (e.g., half-log diluted from 316 to 1 nM), and then exposed to a detection reagent (e.g., using a CELLTITER-GLO® Cell Viability Assay kit) to determine cell viability. The combination activity can be assessed by the Bliss independence model: negative values as indication of antagonism, positive as synergy, and a value of zero as additive activity. Bliss scores in the dose matrix can be added up to give a “Bliss sum” value to reflect the overall synergy activity of the compound provided herein, or a pharmaceutically acceptable salt thereof, and the additional therapeutic agent in each cell line. In some embodiments, a cell line that is not dependent on BCL6 and / or that does not have significant expression of BCL6 can be used as a control (e.g., Toledo, H929, MM.1S, or OPM2). As another example, the potency and / or efficacy of a compound provided herein, or a pharmaceutically acceptable salt thereof, can be evaluated in an animal model, for example, a cell line-derived (CDX) xenograft model (e.g., using an established cancer cell line such as DB, DoHH2, OCI-Ly1, OCI-Ly7, RL, Pfeiffer, SU-DHL-5, SU-DHL-6, WSU-DLCL2, REH, BALL-1, RS4;11, SEMK2, KOPN8, NALM-6, KASUMI-2, RCH-ACV, SUP-B15, BV-173, TOM-1, NALM-20, NALM-21, MUTZ-5, or MHH-CALL-4 (e.g., OCI-Ly1, OCI-Ly7, SU- DHL-5, SU-DHL-6, WSU-DLCL2, DB, RL, Pfeiffer, or DoHH2)), a genetically engineered mouse model (GEMM), or a patient-derived xenograft (PDX) model. For example, a PDX model can be run in immunodeficient mice (e.g., athymic nude, outbred homozygous (e.g., Crl:NU(NCr)-Foxn1nu) or Fox Chase SCID (CB17 / Icr-Prkdcscid / IcrIcoCrl) mice). The mice can be female, 6-12 weeks old at tumor implantation and have access to food and water ad libitum. Approximately 70 mg of a tumor can be implanted subcutaneously in the right flank of each mouse. Following implantation, tumors can be measured weekly and once the tumor volumes reach 150-300 mm3, the mice can be randomized into treatment and control groups. In some embodiments, one or more experimental arms can be added to evaluate pharmacokinetics and / or pharmacodynamics. The mice can be treated with a compound provided herein, or a pharmaceutically acceptable salt thereof, (e.g., via IP or PO administration) and optionally an additional therapy or therapeutic agent (e.g., any of the additional therapies or therapeutic agents described herein). Throughout the study, health condition, body weight and tumor volumes of the mice can be recorded on a weekly basis. The mice can be sacrificed at 28 days or when the tumor reaches 1 cm3, and the tumors can be evaluated (e.g., by tumor weight, by tumor volume). At the end of each study the Best Response can be calculated for each treatment arm. Best Response is defined as the minimum value of ∆Volumet for t ≥ 10 days. Best Responses between the control arm(s) and the treatment arm(s) can be compared to determine if the treatment(s) work better than the control(s). In some embodiments, tumor samples can also be collected at the end of each study and relevant proteins (e.g., BCL6) can be measured to determine if the treatment has a better protein modulation profile compared to a control. In some embodiments, tumor samples and / or blood samples can also be collected at the end of each study and analyzed for altered gene expression activity (e.g., altered ARID3A, ARID3B, ATR, B2M, BANK1, BATF, BCL11A, BCL2, BCL2A1, BLIMP1, BMl1, CASP8, CCND1, CCND2, CCR6, CCR7, CD38, CD44, CD69, CDKN1A, CDKN1B, CFLAR / FLIP, CHEK1, CXCR4, CXCR5, DR5, EBI2, ETV6, FCMR, FGD4, ID2, IFITM1, IFITM2, IFNAR2, IFNGR1, IL10, IL10RB, IL7R, CXCL10, IRF1, IRF4, IRF7, IRF9, JAK3, JARID2, JUN, KLF2, LITAF, MCL1, MIP-1a, MYC, MYD88, NFKBIE, NOTCH2, PDL1, PIM1, PPP3R1, PRDM1, PTEN, S1PR1, SHP1, STAT1, STAT3, STAT5A, TLR1, TLR4, TLR7, TLR9, TNF- R2, TOX, TP53, ZEB2, and / or ZNF608 expression levels). For pharmacokinetic and pharmacodynamic studies, tumor and / or blood samples from the mice can be obtained at the same or different time points than efficacy studies. For example, for pharmacokinetic and pharmacodynamic studies, tumor and / or blood samples from the mice can be obtained at Day 1, 3 and / or 5, with collections at 6, 12 and / or 24 hours post-dosing, and relevant proteins can be measured in the tumor samples and pharmacokinetic studies can be performed on the blood samples or a portion thereof (e.g., plasma). In some embodiments, the PDX is a model of B cell acute lymphoblastic leukemia (B-ALL) (e.g., Philadelphia chromosome positive B-ALL, Philadelphia chromosome negative B-ALL, or B-ALL with an MLL-Af4 fusion, an MLL-Af6 fusion, an MLL-Af9 fusion, an MLL-ENL fusion, or an MLL-PTD fusion), non-Hodgkin lymphoma (e.g., a mature B cell neoplasm (e.g., Burkitt lymphoma (BL), large B cell lymphoma (e.g., diffuse large B-cell lymphoma not otherwise specified (DLBCL-NOS), diffuse large B-cell lymphoma / high grade B cell lymphoma (HGBCL) (e.g., HGBCL with MYC and / or BCL2 rearrangements (HGBCL-MYC / BCL-2)), primary large B cell lymphoma of immune-privileged sites (primary LBCL of immune-privileged sites), intravascular large B- cell lymphoma (IVLBCL), primary mediastinal large B cell lymphoma (primary mediastinal LBCL), or high grade B-cell lymphoma NOS (HBGCL-NOS)), follicular lymphoma (FL), mantle cell lymphoma (MCL), or transformations of indolent B cell lymphomas), a peripheral T-cell lymphoma (PTCL) (e.g., anaplastic large cell lymphoma (ALCL) (e.g., ALK-positive anaplastic large cell lymphoma, or ALK-negative anaplastic large cell lymphoma), nodal T follicular helper cell lymphoma (e.g., nodal T follicular helper cell lymphoma angioimmunoblastic type (also known as angioimmunoblastic T-cell lymphoma (AITL) or follicular helper T-cell lymphoma, angioimmunoblastic type), nodal T follicular helper cell lymphoma follicular type (also known as follicular helper T-cell lymphoma, follicular type), or nodal T follicular helper cell lymphoma NOS (also known as follicular helper T-cell lymphoma, NOS))), or a primary cutaneous T-cell lymphoid proliferation or lymphoma (cutaneous T-cell lymphoma (CTCL)) (e.g., primary cutaneous CD4-positive small or medium T-cell lymphoproliferative disorder, mycosis fungoides, Sezary syndrome (also known as Sézary syndrome), or primary cutaneous gamma-delta T-cell lymphoma)). See, e.g., Guo, Weikai, et al., Journal of Medicinal Chemistry 63.2 (2020): 676-695, doi: 10.1021 / acs.jmedchem.9b01618; and Alaggio, Rita, et al. Leukemia 36.7 (2022): 1720-1748, doi: 10.1038 / s41375-022-01620-2. In some embodiments, the compounds provided herein, or pharmaceutically acceptable salts thereof, exhibit activity in a model of an autoimmune disease or condition. Exemplary assays can be found in, for example, International Publication Nos. WO 2020 / 014599 and WO 2021 / 074620. In some embodiments, a compound provided herein, or pharmaceutically acceptable salt thereof, can be assessed for its ability to modulate (e.g., decrease) Ig antibody production (e.g., IgA antibody production, IgE antibody production, and / or IgG antibody production), modulate (e.g., decrease) Ig antibody affinity (e.g., IgA antibody affinity, IgE antibody affinity, and / or IgG antibody affinity), and / or modulate (e.g., decrease) germinal center formation in an animal (e.g., a mouse) following challenge with a T cell-dependent antigen (e.g., keyhole limpet haemocyanin (KLH) or sheep red blood cells (SRBC)). For example, KLH can be administered to mice (e.g., C57BL / 6 mice), followed by administration of the compound provided herein, or a pharmaceutically acceptable salt thereof, for a period of time (e.g., 14 days). Following sacrifice, serum samples from the mice can be analyzed for IgG specific for KLH, for example, by ELISA. Similarly, germinal centers can be detected using immunohistological staining using, e.g., peanut agglutinin (PNA). See, e.g., Example 1 of WO 2020 / 014599. In some embodiments, a compound provided herein, or a pharmaceutically acceptable salt thereof, can be assessed for its ability to modulate (e.g., decrease) the number of germinal center B cells in an animal (e.g., mouse) following immunization with an antigen. For example, animals (e.g., mice) can be immunized with specific antigens formulated in adjuvant such as Complete Freund's Adjuvant (CFA) or Alum, and after a period of time (e.g., 8 days), the animals can be sacrificed and the spleens harvested. The spleens can be processed into a suspension and cultured in the presence of a compound provided herein, or pharmaceutically acceptable salt thereof. The cells can then be analyzed, for example, for the number of germinal center B cells (e.g., by flow cytometry using the lineage markers GL7 and CD95). See, e.g., WO 2021 / 074620. In some embodiments, a compound provided herein, or pharmaceutically acceptable salt thereof, can be assessed for its ability to improve or prevent one or more symptoms, biomarkers, or other signs of an autoimmune disease or condition in an animal model of the autoimmune disease or condition. Experimental autoimmune encephalitis (EAE) can be used as an animal model of inflammatory diseases of the CNS, including multiple sclerosis (MS) and neuromyelitis optica. In some cases, EAE can be induced in animals (e.g., mice), for example, via immunization with recombinant human myelin oligodendrocyte glycoprotein (MOG) or a fragment thereof (e.g., MOG1-125), myelin basic protein, and / or proteolipid protein. Following induction of EAE, the animals can be treated with a compound provided herein, or a pharmaceutically acceptable salt thereof. The animals can be evaluated by, for example, EAE severity, B cell depletion, or both. See, e.g., Constantinescu, Cris S., et al. British Journal of Pharmacology 164.4 (2011): 1079- 1106, doi: 10.1111 / j.1476-5381.2011.01302.x; Monson, Nancy L., et al. PloS One 6.2 (2011): e17103, doi: 10.1371 / journal.pone.0017103. In some embodiments, the autoimmune disease or condition is an anti-drug or anti- therapy antibody. In some embodiments, the autoimmune disease or condition is an anti-drug antibody. In some embodiments, the anti-drug antibody is an antibody against an antibody drug (e.g., an anti-TNFα antibody drug). In some embodiments, the autoimmune disease or condition is an anti-therapy antibody. In some embodiments, the anti-therapy antibody is an antibody against an enzyme replacement therapy (e.g., Factor VII replacement therapy, α- galactosidase replacement therapy, or alpha-glucosidase replacement therapy). In some embodiments, the anti-therapy antibody is an antibody against a gene therapy (e.g., AAV-based gene therapy). See, e.g., Vaisman-Mentesh, Anna, et al. Frontiers in Immunology 11 (2020): 1951j, doi: 10.3389 / fimmu.2020.01951; Lenders, Malte, and Eva Brand. Drugs 81.17 (2021): 1969-1981, doi: 10.1007 / s40265-021-01621-y; Rana, Jyoti, Maite Melero Munoz, and Moanaro Biswas. Cellular Immunology (2022): 104641, doi: 10.1016 / j.cellimm.2022.104641; and Butterfield, John SS, et al. Cellular Immunology (2023): 104742, doi: 10.1016 / j.cellimm.2023.104742. In some embodiments, the autoimmune disease or condition is anti-synthetase syndrome. For example, a model of anti-synthetase syndrome, can be induced in susceptible mice (e.g., C57BL / 6, B6.G7, and / or NOD.Idd3 / 5) by immunization with histidyl-tRNA synthetase (e.g., murine histidyl-tRNA synthetase or human histidyl-tRNA synthetase), or a fragment thereof. Treatment with a compound provided herein, or a pharmaceutically acceptable salt thereof, can begin at immunization and continue for a period of time (e.g., short term (e.g., 10-14 days) or long term (e.g., 8-16 weeks)), and then the mice can be sacrificed. The mice can be evaluated, for example, for generation of histidyl-tRNA synthetase-specific antibody (e.g., via immunoprecipitation, ELISA, and / or flow cytometry), tissue (e.g., lung and / or muscle) inflammation (e.g., by pathologist review), or a combination thereof. See e.g., Katsumata, Yasuhiro, et al. Journal of Autoimmunity 29.2-3 (2007): 174-186, doi: 10.1016 / j.jaut.2007.07.005; Ascherman, Dana P. Current Rheumatology Reports 17 (2015), doi: 10.1007 / s11926-015-0532-1; and Konishi, Risa, Yuki Ichimura, and Naoko Okiyama. Immunological Medicine 46.1 (2023): 9-14, doi: 10.1080 / 25785826.2022.2137968. In some embodiments, the autoimmune disease or condition is arthritis (e.g., rheumatoid arthritis or inflammatory arthritis). For example, a mouse model of rheumatoid arthritis, collagen induced arthritis (CIA), can be induced in susceptible mice (e.g., DBA / 1 or HLA-DR) by immunization with type II collagen (CII). Treatment with a compound provided herein, or a pharmaceutically acceptable salt thereof, can begin at immunization and continue for a period of time (e.g., 6 weeks). The mice can be evaluated, for example, for clinical scores (e.g., inflammation of an arthritic limb, foot thickness, paw volume (e.g., using a plethysmometer), or a combination thereof), generation of CII-specific antibody, B cell depletion, or a combination thereof. See e.g., Example 2 of WO 2020 / 014599; Brand, David D., et al. Nature Protocols 2.5 (2007): 1269-1275, doi: 10.1038 / nprot.2007.173. Additional animal models of arthritis (e.g., inflammatory arthritis) are known in the art, such as K / BxN mice. In some embodiments, such mice can be treated with a compound provided herein, or a pharmaceutically acceptable salt thereof, and evaluated, for example, in similar ways to CII- immunized mice, or additionally, titering for autoantibodies, such as those against glucose-6- phosphate isomerase. See, e.g., Huang, Haochu, Christophe Benoist, and Diane Mathis. Proceedings of the National Academy of Sciences 107.10 (2010): 4658-4663, doi: 10.1073 / pnas.1001074107; and Pigott, Elizabeth, and Laura Mandik-Nayak. Arthritis & Rheumatism 64.7 (2012): 2169-2178, doi: 10.1002 / art.34406. In some embodiments, the autoimmune disease or condition is graft-versus-host disease (e.g., chronic graft-versus-host disease). In some cases, an animal model of graft-versus-host disease can be in animals (e.g., mice) conditioned with high-dose cyclophosphamide and lethal total-body irradiation (TBI) rescued with bone marrow optionally including allogeneic splenocytes or purified T cells. Administration of the compound provided herein, or a pharmaceutically acceptable salt thereof, for a period of time can follow. The animals can be evaluated by, for example, pulmonary function tests, by immunohistochemistry to evaluate the presence of autoantibodies, or by examining sections of the spleen for germinal centers, including for example, examining for B cell depletion (e.g., germinal center B cell depletion). See, e.g., Srinivasan, Mathangi, et al. Blood, The Journal of the American Society of Hematology 119.6 (2012): 1570-1580, doi: 10.1182 / blood-2011-07-364414; and Paz, Katelyn, et al. Blood, The Journal of the American Society of Hematology 133.1 (2019): 94-99, doi: 10.1182 / blood-2018-03-839993. See also, e.g., Dubovsky, Jason A., et al. The Journal of Clinical Investigation 124.11 (2014): 4867-4876, doi: 10.1172 / JCI75328. In some embodiments, the autoimmune disease or condition is IgG4-related disease (IgG4-RD). In some cases, an animal model of IgG4-RD can be generated by injecting mice with IgGs (e.g., IgG1 and / or IgG4) derived from human IgG4-RD patients. Such mice can be treated with a compound provided herein, or a pharmaceutically acceptable salt thereof. The animals can be evaluated by measuring, for example, pancreatic and / or salivary tissue damage, B cell depletion, or both. See, e.g., Shiokawa, Masahiro, et al. Gut 65.8 (2016): 1322-1332, doi: 10.1136 / gutjnl-2015-310336. In some cases, an animal model of IgG4-RD can be generated by knock-in of a mutation of Linker for Activation of T cell (LAT), such as LAT Y136F. Such mice can be treated with a compound provided herein, or a pharmaceutically acceptable salt thereof. The animals can be evaluated by measuring, for example, pancreatic and / or salivary tissue damage, B cell depletion, or both. See, e.g., Yamada, Kazunori, et al. PLoS One 13.6 (2018): e0198417, doi: 10.1371 / journal.pone.0198417. In some embodiments, the autoimmune disease or condition is lupus (e.g., lupus erythematosus). In some cases, an animal model of lupus is MRL / lpr mice, which can display high expression of Tfh-associated molecules such as ICOS, PD-1, BCL6, and IL-21 and produce autoantibodies to nuclear components, develop nephritis, arthritis, and skin lesions. Such mice can be treated with a compound provided herein, or a pharmaceutically acceptable salt thereof. The animals can be evaluated by, for example, measuring B cell depletion (e.g., germinal center B cell depletion), identifying the presence and / or severity of glomerulonephritis, autoantibody titers (e.g., anti-RNA antibody titers, anti-nuclear antibody titers, and / or anti-dsDNA antibody titers), IL-21 expression, and / or amount of activated CD4+ T cells. See, e.g., Ahuja, Anupama, et al. The Journal of Immunology 179.5 (2007): 3351-3361, doi: 10.4049 / jimmunol.179.5.3351; Shen, Chunxiu, et al. Journal of Cellular and Molecular Medicine 25.17 (2021): 8329-8337, doi: 10.1111 / jcmm.16785; and Marinov, Anthony D., et al. Arthritis & Rheumatology 73.5 (2021): 826-836, doi: 10.1002 / art.41608. Additional animal models of lupus are known in the art, such as NZB / W mice, which can be treated with a compound provided herein, or a pharmaceutically acceptable salt thereof, and evaluated in similar ways to the MRL / lpr mice. See, e.g., Wang, Wensheng, et al. The Journal of Immunology 192.7 (2014): 3011-3020, doi: 10.4049 / jimmunol.1302003; and Kansal, Rita, et al. Science Translational Medicine 11.482 (2019): eaav1648, doi: 10.1126 / scitranslmed.aav1648. In some embodiments, the autoimmune disease or condition is myasthenia gravis (e.g., muscle-specific tyrosine kinase (MuSK) positive myasthenia gravis). For example, an animal model (e.g., a rat model, a mouse model, or a rabbit model) of MuSK positive myasthenia gravis can be generated by immunizing the animal with a purified chimeric protein containing the ectodomain of MuSK (e.g., the ectodomain of MuSK and the Fc region of IgG1). Following immunization, the animals are treated with a compound provided herein, or a pharmaceutically acceptable salt thereof, and the animals (e.g., rats, mice, or rabbits) can be evaluated, for example, by measuring clinical scores (e.g., grasping and / or lifting of a weight, while looking for tremor, hunched posture, muscle strength, and signs of fatigue), body weight, compound muscle action potential (e.g., using electromyography), anti-MuSK antibodies, B cell depletion, or a combination thereof. See, e.g., Shigemoto, Kazuhiro, et al. The Journal of Clinical Investigation 116.4 (2006): 1016-1024, doi: 10.1172 / JCI21545. As another example, an animal model (e.g., a rat model, a mouse model, or a rabbit model) of MuSK positive myasthenia gravis can be generated by immunizing the animal with a purified protein containing the ectodomain of MuSK (e.g., the ectodomain of MuSK with or without a tag, just as a His-tag). Following immunization, the animals are treated with a compound provided herein, or a pharmaceutically acceptable salt thereof, and the animals (e.g., rats, mice, or rabbits) can be evaluated, for example, by measuring clinical scores (e.g., grasping and / or lifting of a weight, while looking for tremor, hunched posture, muscle strength, and signs of fatigue), body weight, compound muscle action potential (e.g., using electromyography), anti- MuSK antibodies, B cell depletion, or a combination thereof. See, e.g., Mori, Shuuichi, et al. The American Journal of Pathology 180.2 (2012): 798-810, doi: 10.1016 / j.ajpath.2011.10.031; and Reuveni, Debby, et al. Frontiers in Immunology 11 (2020): 403, doi: 10.3389 / fimmu.2020.00403. As another example, an animal model (e.g., a rat model, a mouse model, or a rabbit model) of myasthenia gravis can be generated by immunizing the animal with acetylcholine receptor from Torpedo (e.g., Torpedo californica) or Electrophorus (e.g., Electrophorus electricus) electric organs, or recombinant acetylcholine receptor protein or fragments thereof. Treatment with a compound provided herein, or a pharmaceutically acceptable salt thereof, can begin, for example, approximately 4 weeks after immunization, but can sometimes begin earlier or later. The animals (e.g., rats, mice, or rabbits) can be evaluated, for example, by measuring clinical scores (e.g., grasping and / or lifting of a weight, while looking for tremor, hunched posture, muscle strength, and signs of fatigue), body weight, compound muscle action potential (e.g., using electromyography), anti-acetylcholine receptor antibodies, B cell depletion, or a combination thereof. See, e.g., Mori, Shuuichi, et al. The American Journal of Pathology 180.2 (2012): 798-810, doi: 10.1016 / j.ajpath.2011.10.031; Xin, Ning, et al. Molecular and Cellular Neuroscience 58 (2014): 85-94, doi: 10.1016 / j.mcn.2013.12.006; and Losen, Mario, et al. Experimental Neurology 270 (2015): 18- 28, doi: 10.1016 / j.expneurol.2015.03.010. In some embodiments, the autoimmune disease or condition is multiple sclerosis (MS). In some embodiments, the MS is clinically isolated syndrome (CIS), relapsing-remitting MS (RRMS), primary progressive MS (PPMS), or secondary progressive MS (SPMS). In some embodiments, animal models of MS can be based on EAE, for example, relapsing-remitting EAE in SJL / J mice (e.g., via immunization with proteolipid protein(PLP)139-151), chronic EAE in C57BL / 6J mice (e.g., via immunization with MOG35-55), or EAE in transgenic mice (e.g., via a T cell clone expressing Vα and Vβ chains reacting specifically to MOG35-55, or a B cell heavy chain knock-in mouse). In some embodiments, the animal (e.g., mouse) model is generated via infection with a picornavirus, such as Theiler’s murine encephalitis virus. In some embodiments, the animal (e.g., mouse) model is generated by feeding C57BL / 6 mice with cuprizone (e.g., 0.2% for 6 weeks). In some embodiments, the animal (e.g., mouse) model is generated via lysolecithin injection (e.g., in SJL / J mice). Treatment with a compound provided herein, or a pharmaceutically acceptable salt thereof, can be followed, for example, by analysis of the animals for levels of myelin-specific T cells, B cell depletion, reduction of inflammatory lesions, axonal degeneration, protection or reversal of cuprizone or lysolecithin- induced demyelination, or a combination thereof. See, e.g., Procaccini, Claudio, et al. European Journal of Pharmacology 759 (2015): 182-191, doi: 10.1016 / j.ejphar.2015.03.042. In some embodiments, the autoimmune disease or condition is neuromyelitis optica (NMO). In some cases, animal models of NMO include administration of antibodies against astrocyte water channel aquaporin-4 (AQP4), called AQP4-IgG or NMO-IgG, to various CNS tissues, such as the brain. In some embodiments, the administration of the antibodies is to an animal with EAE. The AQP4-IgG can be recombinant or derived from human NMO patients. Treatment with a compound provided herein, or pharmaceutically acceptable salt thereof, can be followed, for example, by analysis of the sacrificed animal for slowing or reversal of astrocyte demyelination, number of macrophages, number of activated microglia, number of activated neutrophils, B cell depletion, or a combination thereof. See, e.g., Bennett, Jeffrey L., et al. Annals of Neurology: Official Journal of the American Neurological Association and the Child Neurology Society 66.5 (2009): 617-629, doi: 10.1002 / ana.21802; Saini, Harleen, et al. BMC Neurology 13.1 (2013), doi: 10.1186 / 1471-2377-13-104; Oji, Satoru, et al. PloS One 11.3 (2016): e0151244, doi: 10.1371 / journal.pone.0151244; Peschl, Patrick, et al. Journal of Neuroinflammation 14.1 (2017), doi: 10.1186 / s12974-017-0984-5; and Duan, Tianjiao, and Alan S. Verkman. Brain Pathology 30.1 (2020): 13-25, doi: 10.1111 / bpa.12793. In some embodiments, the autoimmune disease or condition is pemphigus (e.g., pemphigus vulgaris). In some cases, an animal (e.g., mouse) model of pemphigus can be generated using adoptive transfer of peripheral lymphocytes from Dsg3 knockout animals to immune-deficient but desmoglein 3-expressing recipient mice to create an artificial immune state in the recipient animals. In some cases, an animal (e.g., mouse) model of pemphigus can be generated using an animal with a MHC class II-null background that expresses the pemphigus-associated HLA-DRB1*0402 allele, which after immunization with recombinant human DSG3, produce anti-human DSG3 antibodies. Treatment of these models with a compound provided herein, or a pharmaceutically acceptable salt thereof, can be followed, for example, by analysis of the B cell repertoires of the animals for anti-desmoglein B-cell clones, B cell depletion, or both. See, e.g., Kasperkiewicz, Michael, et al. Nature Reviews Disease Primers 3.1 (2017): 17071, doi: 10.1038 / nrdp.2017.71. In some embodiments, the autoimmune disease or condition is Sjogren’s syndrome. In some cases, an animal model of Sjogren’s syndrome is a NOD mouse, which sometimes has further genetic manipulation or crosses (e.g., NOD.B10.H2bor C57BL / 6.NOTDc3.NODc1t) to recapitulate the symptoms of the syndrome. Such mice can be treated with a compound provided herein, or a pharmaceutically acceptable salt thereof. The animals can be evaluated, for example, for salivary and lacrimal gland secretory flow rates, salivary protein content, autoantibodies to exocrine gland proteins (e.g., anti-Sjogren’s syndrome A (SSA) antibodies, anti-Sjogren’s syndrome B (SSB) antibodies, and / or anti-muscarinic acetylcholine 3 receptor (M3R) antibodies), B cell depletion, or a combination thereof. Robinson, Christopher P., et al. Arthritis & Rheumatism 41.1 (1998): 150-156, doi: 10.1002 / 1529- 0131(199801)41:1<150::AID-ART18>3.0.CO;2-T; Cha, Seunghee, et al. Arthritis & Rheumatism 46.5 (2002): 1390-1398, doi: 10.1002 / art.10258; and Ohno, Seiji, et al. Autoimmunity 45.7 (2012): 540-546, doi: 10.3109 / 08916934.2012.710860. Additional animal models of Sjogren’s syndrome are known in the art and include, for example, NFS / sld mice, IQI / Jic mice, Aly / aly mice, and mice immunized with M3R peptides, which can be evaluated, in some cases, for the same parameters as NOD mice. See, e.g., Iizuka, Mana, et al. Journal of Autoimmunity 35.4 (2010): 383-389, doi: 10.1016 / j.jaut.2010.08.004; and Park, Young-Seok, Adrienne E Gauna, and Seunghee Cha. Current Pharmaceutical Design 21.18 (2015): 2350- 2364, doi: 10.2174 / 1381612821666150316120024. The pharmacokinetic parameters of a compound provided herein, or a pharmaceutically acceptable salt thereof, can be evaluated in an animal model, for instance, a mouse model, a rat model, a dog model, or a nonhuman primate (e.g., cynomolgus monkey) model. Pharmacokinetics (PK) studies can be conducted in an animal model (e.g., male CD-1 mice) by two exemplary delivery routes: intravenous (IV) injection and oral (PO), for example, oral gavage. Animals in the IV group (e.g., n = 3) are allowed free access to food and water; animals in the PO group are allowed free access to food or are fasted for 6-8 hours prior to dosing. A compound provided herein, or a pharmaceutically acceptable salt thereof, can be formulated in solution for the IV route and solution or suspension for the PO route. On each dosing day of the experiment, the compound provided herein, or a pharmaceutically acceptable salt thereof, can be administered via vein injection (e.g., at 1 mg / kg) for IV route or via oral gavage (e.g., at 3 to 300 mg / kg, at 3 to 90 mg / kg, or 3 to 10 mg / kg, such as 10 mg / kg or 30 mg / kg) for PO route. In some cases, the animals can be orally pre-dosed with a cytochrome P450 inhibitor (e.g., 1-aminobenzotriazole) prior to (e.g., 16 hours prior to) dosing the compound provided herein, or a pharmaceutically acceptable salt thereof. Blood samples can be collected via serial bleeding at multiple timepoints (e.g., at 8 timepoints from 0.83 to 24 hours post dose for a single-dose study). At each timepoint, blood (it will be understood that the volume of the blood sample will vary based on species) can be collected (e.g., via a vein, such as the saphenous vein in mice) in a tube containing an anti-coagulant (e.g., K2EDTA). Blood samples can be put on wet ice and centrifuged (e.g., at 2000 x g for 4-10 minutes) to obtain plasma samples. Plasma samples can be diluted (e.g., with an equal volume of pH 3.0 phosphate buffer or with an equal volume of pH 5.0 sodium citrate) and submitted to LC-MS / MS for sample analysis. Pharmacokinetics parameters, including clearance (CL), volume of distribution (Vd), maximum plasma concentration (Cmax), time of maximum plasma concentration (tmax), half- life (t1 / 2), area under the curve (AUC), and oral bioavailability (%F) can be calculated using a non-compartmental model. In some embodiments, the pharmacokinetic parameters of a compound provided herein, or a pharmaceutically acceptable salt thereof, can be measured in a rat model (e.g., a Sprague- Dawley rat model). An exemplary protocol follows. Rats (e.g., male Sprague-Dawley rats, 7-9 weeks of age) are dosed with a compound provided herein, or a pharmaceutically acceptable salt thereof, once per day orally (e.g., via gavage) for several days (e.g., 3 days). The compound provided herein, or a pharmaceutically acceptable salt thereof, is administered to the rats at a given dose level (e.g., 1, 3, 5, 10, 25, 30, 50, or 100 mg / kg) in a solution or suspension formulation (e.g., 10% DMA / 45% PHOSAL 50 PG / 40% MIGLYOL® 810 N / 5% polysorbate 80). The rats have access to food and water ad libitum. Blood samples (e.g., 150 µL per sample) from the rats are taken at predetermined intervals, such as 1, 4, 8, 12, 24, 38, 49, 52, 60, 72, 96, and / or 120 hours after the first dose is administered. The blood is sampled via jugular vein puncture, then the blood samples (e.g., with K2EDTA as anticoagulant) are temporarily put on ice and then centrifuged (e.g., at 4 °C and 6000 RPM for 5 minutes) within 30 minutes. Plasma samples are put on dry ice. After the completion of the last sampling, all samples are stored at -80°C or analyzed in a short time following collection. The concentration of the compound provided herein, or a pharmaceutically acceptable salt thereof, can be measured in an acidified plasma sample (e.g., diluted 1:1 v / v with pH 3 phosphate buffer) can be determined (e.g., via LC / MS / MS). For example, an acidified plasma sample is prepared for analysis using protein precipitation (e.g., by the addition of methanol), and an internal standard is spiked in at a known concentration. The spiked sample is mixed, centrifuged, and the supernatant is used in an LC / MS / MS method. The LC / MS / MS method uses a KINETEX® C182.6 μm 100 Å (50 mm * 2.10 mm) column with a first mobile phase of water (0.1% formic acid (FA)) and a second mobile phase of acetonitrile (0.1% FA). Multiple reaction monitoring is used to measure the analyte(s) of interest. Using the concentration of the compound provided herein, or a pharmaceutically acceptable salt thereof, in the plasma sample, pharmacokinetic parameters of t1 / 2 (hr), tmax (hr), Cmax(ng / mL), AUClast(hr*ng / mL), AUCInf(hr*ng / mL), AUCExtr(%), MRTInf(hr), AUCInf / D (hr*kg*ng / mL / mg), %F, AUC0-24 (hr*ng / mL), and AUC48-72 (hr*ng / mL) are determined. At least one blood sample (e.g., taken at 72 hours after the first dose) is used for clinical chemistry, and levels of one or more of TBA (μmol / L), AST (U / L), ALT (U / L), GLU (mmol / L), ALP (U / L), BUN (mmol / L), CREA (μmol / L), CHOL (mmol / L), TG (mmol / L), CK (U / L), Ca (mmol / L), P (mmol / L), TBIL (μmol / L), ALB (g / L), TP (g / L), K (mmol / L), Na (mmol / L), Cl (mmol / L), A / G, and GLB (g / L) are determined. The clinical observations, body weight and food consumption of the rats are tracked during dosing, and also for three days after the cessation of dosing. The rats are then sacrificed and grossly assessed for any macroscopic abnormalities. In some embodiments, the pharmacokinetic parameters of a compound provided herein, or a pharmaceutically acceptable salt thereof, can be measured in a mouse model (e.g., a Balb / c model). An exemplary protocol follows. Mice (e.g., male Balb / c mice, 9-11 weeks of age) are dosed with a compound provided herein, or a pharmaceutically acceptable salt thereof, twice per day orally (e.g., via gavage) for several days (e.g., 10 days). The compound provided herein, or a pharmaceutically acceptable salt thereof, is administered to the mice at a given dose level (e.g., 1, 3, 5, 10, 25, 30, 50, or 100 mg / kg) in a solution or suspension formulation (e.g., 10% DMA / 45% PHOSAL 50 PG / 40% MIGLYOL® 810 N / 5% polysorbate 80). The mice have access to food and water ad libitum. Blood samples (e.g., 30 µL per sample) from the mice are taken at predetermined intervals, such as 14, 12, 16, 24, 64, 136, 220, 228, 232, and 240 hours after the first dose is administered (not every mouse will have every time point sampled). The blood is sampled via saphenous vein puncture, then the blood samples (e.g., with K2EDTA as anticoagulant) are temporarily put on ice and then centrifuged (e.g., at 4 °C and 4600 RPM for 5 minutes) within 30 minutes. Plasma samples are acidified and put on dry ice. After the completion of the last sampling, all samples are stored at -80°C or analyzed in a short time following collection. The concentration of the compound provided herein, or a pharmaceutically acceptable salt thereof, measured in an acidified plasma sample (e.g., diluted 1:1 v / v with pH 3 phosphate buffer) can be determined (e.g., via LC / MS / MS). For example, an acidified plasma sample is prepared for analysis using protein precipitation (e.g., by the addition of acetonitrile), and an internal standard is spiked in at a known concentration. The spiked sample is mixed, centrifuged, and the supernatant is used in an LC / MS / MS method. The LC / MS / MS method uses an ACQUITY UPLC BEH C181.7μm (2.1*50 mm) column with a first mobile phase of 5 mM NH4OAC (0.05% FA or 0.1% FA) and a second mobile phase of acetonitrile (0.1% FA). Multiple reaction monitoring is used to measure the analyte(s) of interest. Using the concentration of the compound provided herein, or a pharmaceutically acceptable salt thereof, in the plasma sample, pharmacokinetic parameters of t1 / 2(hr), tmax(hr), Cmax(ng / mL), AUClast(hr*ng / mL), AUCInf(hr*ng / mL), AUCExtr(%), MRTInf(hr), AUCInf / D (hr*kg*ng / mL / mg), and %F, are determined. The clinical observations, body weight and food consumption of the mice are tracked during dosing, and also for three days after the cessation of dosing. The mice are then sacrificed and grossly assessed for any macroscopic abnormalities. In some embodiments, the %F for a compound provided herein, or a pharmaceutically acceptable salt thereof, is at least 4%. In some embodiments, the %F for a compound provided herein, or a pharmaceutically acceptable salt thereof, is at least 10%. In some embodiments, the %F for a compound provided herein, or a pharmaceutically acceptable salt thereof, is at least 20%. In some embodiments, the %F for a compound provided herein, or a pharmaceutically acceptable salt thereof, is at least 30%. In some embodiments, the %F for a compound provided herein, or a pharmaceutically acceptable salt thereof, is at least 40%. In some embodiments, the %F for a compound provided herein, or a pharmaceutically acceptable salt thereof, is at least 60%. In some embodiments, the %F for a compound provided herein, or a pharmaceutically acceptable salt thereof, is at least 80%. In some embodiments, the %F for a compound provided herein, or a pharmaceutically acceptable salt thereof, is about 4% to about 90% (e.g., about 4% to about 80%, about 4% to about 60%, about 4% to about 40%, about 4% to about 20%, about 4% to about 10%, about 20% to about 40%, about 40% to about 60%, about 60% to about 80%, or about 70% to about 90%). In some embodiments, the %F for a compound provided herein, or a pharmaceutically acceptable salt thereof, is about 4% to about 20%. In some embodiments, the %F for a compound provided herein, or a pharmaceutically acceptable salt thereof, is about 20% to about 40%. In some embodiments, the %F for a compound provided herein, or a pharmaceutically acceptable salt thereof, is about 40% to about 60%. In some embodiments, the %F for a compound provided herein, or a pharmaceutically acceptable salt thereof, is about 50% to about 80%. In some embodiments, a compound provided herein, or a pharmaceutically acceptable salt thereof, is not a substrate of a human cytochrome P450 enzyme. In some embodiments, a compound provided herein, or a pharmaceutically acceptable salt thereof, is not a substrate of a human cytochrome P450 enzyme where ≥ 25% of clearance is attributed to that enzyme. In some embodiments, a compound provided herein, or a pharmaceutically acceptable salt thereof, is not an inhibitor and / or an inducer of one or more human cytochrome P450 enzymes. In some embodiments, a compound provided herein, or a pharmaceutically acceptable salt thereof, is not an inhibitor and / or an inducer of one or more human cytochrome P450 enzymes, where the IC50 and / or EC50 for the one or more human cytochrome P450 enzymes, respectively, is at a concentration to be significantly greater than the estimated free fraction concentration of a compound provided herein, or a pharmaceutically acceptable salt thereof, at a clinically relevant dose. Exemplary human cytochrome P450 enzymes include those in the CYP1, CYP2, and CYP3 families. Of those CYP1A1, CYP1A2, CYP1B1, CYP2A6, CYP2B6, CYP2C8, CYP2C9, CYP2C18, CYP2C19, CYP2D6, CYP2J2, CYP2S1, CYP2E1, CYP3A4, and CYP3A5 are known drug metabolizing enzymes. In some embodiments, no single cytochrome P450 enzyme is responsible for greater than or equal to 25% of the elimination of a compound provided herein, or a pharmaceutically acceptable salt thereof. Cytochrome P450 inhibition and / or inducing activity can be determined using appropriate in vitro assays, such as those described in the guidance document “In Vitro Drug Interaction Studies — Cytochrome P450 Enzyme- and Transporter-Mediated Drug Interactions” provided by the U.S. F.D.A. in January 2020, and similarly in the ICH M12 guidance finalized in May 2024. For example, evaluation of cytochrome P450 inhibition can be performed in in vitro studies, in both a reversible and time-dependent manner. In an in vitro inhibition study, the ratio of intrinsic clearance values of a probe substrate for an enzymatic pathway in the absence and in the presence of a compound provided herein, or a pharmaceutically acceptable salt thereof, can be calculated based on these in vitro results; this ratio is referred to as R1for reversible inhibition, where R1= 1 + (Imax,u / Ki,u), and Imax,uis the maximal unbound plasma concentration of the compound provided herein, or a pharmaceutically acceptable salt thereof, predicted in human, and Ki,u is the unbound inhibition constant determined in vitro. Specifically, in the case of CYP3A whereas the enzyme is also expressed at significant levels in the intestine, R1,gutcan be calculated where R1,gut= 1 + (Igut + Ki,u),and where Igut is predicted human intestinal luminal concentration of the compound provided herein, or a pharmaceutically acceptable salt thereof, calculated as the human oral dose / 250mL. The time-dependent inhibition ratio R2can similarly be calculated, where R2= (kobs+ kdeg) / kdeg, and kobs is the observed (apparent first order) inactivation rate of the affected cytochrome P450 calculated by kobs = (kinact*Imax,u) / (KI,u + *Imax,u), kdeg is the apparent first- order degradation rate constant of the affected cytochrome P450, KI,u is the unbound concentration of the compound provided herein, or a pharmaceutically acceptable salt thereof, causing half maximal inactivation, and kinact is the maximal inactivation rate constant. Utilizing these equations for R1, R1,gut, and R2, the compound provided herein, or a pharmaceutically acceptable salt thereof, can be evaluated for their potential to be an inhibitor of a cytochrome P450, and the drug-drug interaction (DDI) potential can be further investigated using mechanistic or physiological-based pharmacokinetic models of the liver and intestine and / or conducting a clinical DDI study with a sensitive index substrate. Additionally, a compounds propensity to activate nuclear receptors (e.g., PXR, CAR, or AhR) is evaluated through in vitro cytochrome P450 hepatocyte induction studies and the resulting data can be evaluated via the fold-change method, wherein the fold-change in cytochrome P450 enzyme mRNA levels, when incubated with the compound provided herein, or a pharmaceutically acceptable salt thereof, based on cutoff determined from known positive and negative controls to calibrate the system. For example, a compound provided herein, or a pharmaceutically acceptable salt thereof, is determined an inducer if: (1) it increases mRNA expression of a cytochrome P450 enzyme in a concentration-dependent manner; and (2) the fold change of cytochrome P450 mRNA expression relative to the vehicle control is ≥ 2-fold at the expected hepatic concentrations of the drug. Additionally, evaluation of cytochrome P450 induction can be performed by a correlation method, wherein correlation methods are used to predict the magnitude of a clinical induction effect (e.g., AUC ratio of an index substrate in the presence and absence of inducers) of a compound provided herein, or a pharmaceutically acceptable salt thereof, according to a calibration curve of relative induction scores (RIS) or Imax,u / EC50for a set of known inducers of the same cytochrome P450. If the predicted magnitude is more than a predefined cut-off (e.g., AUC ratio ≤ 0.8), a compound provided herein, or a pharmaceutically acceptable salt thereof, is considered to have induction potential in vivo. In some embodiments, a compound provided herein, or a pharmaceutically acceptable salt thereof, can be tested for its potency in inhibiting hERG potassium channels. The cardiac potassium channel hERG is responsible for a rapid delayed rectifier current (IKr) in human ventricle and inhibition of IKris the most common cause of cardiac action potential prolongation by non-cardiac drugs. Increased action potential duration causes prolongation of the QT interval that has been associated with a dangerous ventricular arrhythmia, torsade de pointes. There are several methods of testing hERG inhibition potency, including Fastpatch hERG and manual patch clamp experiments. In some embodiments, a compound provided herein, or a pharmaceutically acceptable salt thereof, is tested for its potency in inhibiting hERG potassium channels using a manual patch clamp assay. For example, in some embodiments, solutions or suspensions of a compound provided herein, or a pharmaceutically acceptable salt thereof, at several concentrations (e.g., 0.3, 1, 3 and 10 µM) can be exposed to single cells. The effect of the compound provided herein, or a pharmaceutically acceptable salt thereof, on the inhibition of hERG potassium channels can be measured in this system using an electrical pulse pattern, the data plotted, and an IC50 value calculated for the inhibition of hERG by the compound provided herein, or a pharmaceutically acceptable salt thereof. An exemplary protocol follows. In this experiment, hERG potassium channels are expressed in a human embryonic kidney cell line that lacks endogenous IKr (HEK-293 (ATCC 293T, CRL-3216™)). See, e.g., Brown, Arthur M., and David Rampe. Pharmaceutical News 7.4 (2000): 15-20; Weirich, Jörg, and H. Antoni, Basic Research in Cardiology 93 (1998): s125-s132, doi: 10.1007 / s003950050236; and Yap, Yee Guan, and A. J. Camm. Clinical & Experimental Allergy 29 (1999): 174-181, doi: 10.1046 / j.1365-2222.1999.0290s3174.x. All chemicals used in solution preparations are purchased from a commercial supplier (e.g., Sigma-Aldrich) and are of ACS reagent grade purity or higher. Stock solutions of the compound provided herein, or a pharmaceutically acceptable salt thereof, positive control compound(s), and reference substance(s) are prepared in dimethyl sulfoxide (DMSO) and stored frozen. Solutions of each compound provided herein, or a pharmaceutically acceptable salt thereof, positive control compound, and reference substance concentrations are prepared fresh daily by diluting stock solutions into HEPES-buffered physiological saline solution (HB- PS; 137 mM NaCl, 4 mM KCl, 1.8 mM CaCl2, 1 mM MgCl2, 10 mM HEPES, and 10 mM glucose, pH 7.4). Since previous results have shown that ≤ 0.3% DMSO does not affect channel current, all test and control solutions can contain 0.3% DMSO. In some embodiments, a positive control compound can be included in the experiment. In some such embodiments, the positive control compound can be terfenadine (Sigma-Aldrich), for example, in a HB-PS and 0.3% DMSO solution. In some embodiments, a reference compound can be included in the experiment. In some such embodiments, the reference compound can be E-4031 (Sigma-Aldrich), for example, in a HB-PS and 0.3% DMSO solution. If necessary, test article solutions are sonicated to facilitate dissolution. Visible precipitate observed during preparation or exposure of test article formulations to the test system is noted for reference. The effect of a compound provided herein, or a pharmaceutically acceptable salt thereof, are initially evaluated at concentration range of 1 to 10 µM. Subsequent concentrations are evaluated based on the inhibition observed at that concentration. HEK-293 cells are transfected with hERG cDNA. Stable transfectants are selected by coexpression of the G418-resistance gene incorporated into the expression plasmid. Selection pressure is maintained by including G418 in the culture medium. Cells are cultured in Dulbecco’s Modified Eagle’s Medium / Ham’s Nutrient Mixture F-12 (DMEM / F-12) supplemented with 10% fetal bovine serum and the appropriate concentrations of penicillin G sodium, streptomycin sulfate, and G418. All experiments are performed at near-physiological temperature (33 – 35 °C). Each cell acts as its own control. The effect of a compound provided herein, or a pharmaceutically acceptable salt thereof, is evaluated at multiple (e.g., up to four) concentrations. Each concentration will be tested in at least three cells (n ≥ 3). Additional concentration(s) may be tested due to the limits imposed by the physiochemical effects of the compound provided herein, or a pharmaceutically acceptable salt thereof (e.g., solubility or cytotoxicity). The positive control compound is tested in at least two (2) cells (n ≥ 2). Cells are transferred to the recording chamber and superfused with vehicle control solution. Pipette (intracellular) solution for whole cell recordings is composed of 130 mM potassium aspartate, 5 mM MgCl2, 5 mM EGTA, 4 mM ATP, and 10 mM HEPES, pH 7.2. Pipette solution is prepared in batches, aliquoted, stored frozen and a fresh aliquot thawed each day. The recording is performed at a temperature of 33 to 35 °C using a combination of in-line solution pre-heater, chamber heater, and feedback temperature controller. Temperature is measured using a thermistor probe in the recording chamber. Micropipettes for patch clamp recording are made from glass capillary tubing using a P-97 micropipette puller (Sutter Instruments). A commercial patch clamp amplifier (Molecular Devices) is used for whole patch clamp cell recordings. Before digitization, current records are low-pass filtered. Cells stably expressing hERG are held at -80 mV. Onset and steady state inhibition of hERG potassium current due to the compound provided herein, or a pharmaceutically acceptable salt thereof, are measured using a pulse pattern with fixed amplitudes (conditioning prepulse of +20 mV for 1 second; repolarizing test ramp to –80 mV (at –0.5 V / second) repeated at 5 second intervals). Each recording ends with an application of a supramaximal concentration of the reference substance (e.g., E-4031 at 500 nM) to assess the contribution of endogenous currents. The remaining uninhibited current is subtracted off-line digitally from the data to determine the potency of the compound provided herein, or a pharmaceutically acceptable salt thereof, for hERG inhibition. Peak current is measured during the test ramp. A steady state is maintained for at least 20 seconds before applying the compound provided herein, or a pharmaceutically acceptable salt thereof, positive control compound, or reference substance. Peak tail currents are measured until a new steady state is achieved. If a steady state cannot be reached within 12 minutes, the response at 12 minutes is substituted for the steady state value and a notation made. Data acquisition and analyses are performed using the commercial suite of pCLAMP programs (Molecular Devices). Steady state is defined by the limiting constant rate of change with time (linear time dependence). The steady state before and after application of each compound provided herein, or a pharmaceutically acceptable salt thereof, is used to calculate the percentage of current inhibited at each concentration. In some embodiments, a compound provided herein, or a pharmaceutically acceptable salt thereof, is tested for its potency in inhibiting hERG potassium channels (e.g., encoded by the KCNH2 gene and expressed in HEK293 cells) using a Fastpatch hERG assay. For example, in some embodiments, solutions or suspensions of a compound provided herein, or a pharmaceutically acceptable salt thereof, at several concentrations (e.g., 0.3, 1, 3 and 10 µM) can be exposed to cells in an automatic parallel patch clamp system. The effect of the compound provided herein, or a pharmaceutically acceptable salt thereof, on the inhibition of hERG potassium channels can be measured in this system using an electrical pulse pattern, the data plotted, and an IC50 value calculated for the inhibition of hERG by the compound provided herein, or a pharmaceutically acceptable salt thereof. An exemplary protocol follows. The in vitro effects of a compound provided herein, or a pharmaceutically acceptable salt thereof, are evaluated at room temperature using the QPATCH HT® (Sophion Bioscience A / S, Denmark), an automatic parallel patch clamp system. The compound provided herein, or a pharmaceutically acceptable salt thereof, is exposed to hERG at 0.3, 1, 3 and 10 µM in at least five cells (n ≥ 5). The duration of exposure to each compound concentration is at least three minutes. Solutions or suspensions of the compound(s) provided herein, or a pharmaceutically acceptable salt thereof, are prepared daily. Various concentrations are prepared by diluting stock solutions into an appropriate HEPES-buffered physiological saline solution (HB-PS). Previous results have shown that 0.3% DMSO does not affect channel current. Therefore, all test and control solutions can contain up to 0.3% DMSO. Each formulation of a compound provided herein, or a pharmaceutically acceptable salt thereof, can be sonicated (e.g., Model 2510 / 5510, Branson Ultrasonics, Danbury, CT), e.g., at room temperature, to facilitate dissolution. In some embodiments, a positive control can be included in the experiment. In some such embodiments, the positive control compound can be cisapride (Tocris Bioscience), for example, in a 0.3% DMSO solution. In preparation for the recording session, a glass-lined 96-well compound plate is loaded with the appropriate amounts of solutions of compound(s) provided herein, or a pharmaceutically acceptable salt thereof, and control solutions, and placed in the plate well of the QPATCH® (Sophion Bioscience A / S, Denmark). HEK293 (ATCC 293T, CRL-3216™) cells are stably transfected with the appropriate ion channel cDNA(s). Except for cells that have been stored frozen, stable transfectants are maintained in the culture medium with the appropriate selection pressure and antibiotics. All experiments are performed at room temperature. Each cell acts as its own control. Vehicle is applied via the QPATCH® robot pipetting system to naive cells for a 5-10 minute exposure interval. After vehicle application, various concentrations of a compound provided herein, or a pharmaceutically acceptable salt thereof, are applied in at least three (3) minute intervals (n ~ 3, where n = the number of cells / concentration). Each solution exchange on the QPATCH® is performed multiple times, which results in 100% replacement of the compound in the QPlate. Positive control(s) are applied in the same manner as the compound provided herein, or a pharmaceutically acceptable salt thereof, to verify sensitivity to ion channel blockade. In preparation for a recording session, an intracellular solution (e.g., 137 mM NaCl, 4 mM KCl, 1.8 mM CaCl2, 1 mM MgCl2, 10 mM HEPES, and 10 mM glucose, pH 7.4) is loaded into the intracellular compartments of the QPlate and cell suspension is pipetted into the extracellular compartments. After establishment of a whole-cell configuration, membrane currents are recorded using up to 48 parallel patch clamp amplifiers in the QPATCH® system. Valid whole-cell recordings meet the following criteria: 1. Membrane resistance ≥ 200 MΩ. 2. Leak current ≤ 25% channel current or subtracted. Onset and block of hERG current is measured using a stimulus voltage pattern consisting of a 500 ms prepulse to -40 mV (leakage subtraction), a 2-second activating pulse to +40 mV followed by a 2-second test pulse to -40 mV. The pulse pattern is repeated continuously at 10 s intervals from a holding potential of -80 mV. Peak tail current is measured during the -40 mV test pulse. Leakage current is calculated from the current amplitude evoked by the -40 mV prepulse and subtracted from the total membrane current record. Data acquisition and analyses are performed using conventional software. Steady state is defined by the limiting constant rate of change with time (linear time dependence). The steady state before and after application of a compound provided herein, or a pharmaceutically acceptable salt thereof, will be used to calculate the percentage of current inhibited at each concentration. If current is blocked ≥50%, estimated IC50 values will be calculated using the following formula: % Inhibition = {1-1 / [l+([Test] / IC50)N]}*100 Where [Test] is the concentration of the compound provided herein, or a pharmaceutically acceptable salt thereof, IC50is the concentration of the compound provided herein, or a pharmaceutically acceptable salt thereof, at half-maximal inhibition, N is the Hill coefficient, and % Inhibition is the percentage of current inhibited at each test article concentration. Nonlinear least squares fits are solved with the Solver add-in for Excel (Microsoft, WA). Overestimation of current inhibition, due to rundown, is avoided by a manual adjustment that uses an exponential compensation formula in the QPATCH® analysis software. In some embodiments, a compound provided herein, or a pharmaceutically acceptable salt thereof, is not a hERG inhibitor. In some embodiments, a compound provided herein, or a pharmaceutically acceptable salt thereof, inhibits hERG with an IC50of greater than 60 nM (e.g., greater than 100 nM, 300 nM, 500 nM, 1 µM, 3 µM, 5 µM, 10 µM, 20 µM, or 30 µM). For example, a compound provided herein, or a pharmaceutically acceptable salt thereof, inhibits hERG with an IC50of greater than 500 nM (e.g., greater than 1 µM, 3 µM, 5 µM, 10 µM, 20 µM, or 30 µM). In some embodiments, a compound provided herein, or a pharmaceutically acceptable salt thereof, inhibits hERG with an IC50 of greater than 1 µM (e.g., greater than 3 µM, 5 µM, 10 µM, 20 µM, or 30 µM). In some embodiments, a compound provided herein, or a pharmaceutically acceptable salt thereof, inhibits hERG with an IC50of greater than 10 µM (e.g., greater than 20 µM or 30 µM). In some embodiments, a compound provided herein, or a pharmaceutically acceptable salt thereof, inhibits hERG with an IC50 of greater than 30 µM. In some embodiments, a compound provided herein, or a pharmaceutically acceptable salt thereof, can be evaluated for potential secondary pharmacology. For example, in some embodiments, solutions of a compound provided herein, or a pharmaceutically acceptable salt thereof, at a single or several concentrations can be exposed to a panel of primary cells, cell lines or isolated tissues expressing known pharmacological receptors, enzymes or transporters. The effect of the compound provided herein, or a pharmaceutically acceptable salt thereof, the secondary pharmacological target of interest can be determined, the data is initially plotted as a percent inhibition. For secondary targets exceeding an inhibition threshold (typically ≥ 50%), an IC50 value is generated and calculated following an 8-point concentration curve of the compound provided herein, or a pharmaceutically acceptable salt thereof. An exemplary list of assays is included in Table 1 below. One or more of these assays can be used to assess the secondary pharmacological characteristics of a compound provided herein. Exemplary protocols are described in Valentin, Jean-Pierre, and Tim Hammond. Journal of Pharmacological and Toxicological Methods 58.2 (2008): 77-87; doi: 10.1016 / j.vascn.2008.05.007; Wakefield, Ian D., et al. Fundamental & Clinical Pharmacology 16.3 (2002): 209-218, doi: 10.1046 / j.1472-8206.2002.00099.x; Whitebread, Steven, et al. Drug Discovery Today 10.21 (2005): 1421-1433, doi: 10.1016 / S1359- 6446(05)03632-9; and Lounkine, Eugen, et al. Nature 486.7403 (2012): 361-367, doi: 10.1038 / nature11159. Table 1.

[0003] In some embodiments, a compound provided herein, or a pharmaceutically acceptable salt thereof, can be evaluated for potential to induce phospholipidosis. For example, in some embodiments, solutions or suspensions of a compound provided herein, or a pharmaceutically acceptable salt thereof, at several concentrations can be exposed to cells in a dye-based assay using a dye that binds to phospholipids. The effect of the compound provided herein, or a pharmaceutically acceptable salt thereof, on the accumulation of phospholipids can be determined, the data plotted, and an IC50value calculated for Cell Loss due to phospholipidosis by the compound provided herein, or a pharmaceutically acceptable salt thereof. An exemplary protocol follows. HepG2 culture medium is prepared by supplementing Dulbecco’s Modified Eagle’s Medium (DMEM) low glucose media with 1% 2-[4-(2-hydroxyethyl)piperazin-1- yl]ethanesulfonic acid (HEPES), 10% Fetal bovine serum (FBS), 1% non-essential amino acids (NEAA) and 1% of a penicillin, streptomycin mixture (PS). HepG2 cells are cultivated (e.g., in T-75 flasks in a cell culture incubator set at 37 °C, 5% CO2, 95% relative humidity). Cells are allowed to reach 80-90% confluence before detaching and splitting. The HepG2 culture medium is aspirated from the HepG2 cells (e.g., from a T75 flask) and 10 mL of phosphate buffer is added, and the cells are washed two times. The phosphate buffer is aspirated, 3-5 mL of Trypsin-EDTA is added, and the flask is incubated at 37 °C for 5 min. Once the cells are detached, a 3-fold volume of HepG2 culture medium is added into the flask to neutralize the trypsin effect, and the flask contents are transferred to 50 mL vial. The vial with cells is centrifuged (e.g., at 150 × g for 5 min at room temperature). The supernatant is aspirated carefully, and the cell pellet is re-suspended with culture medium. The cell density is adjusted to 6×104cells / mL and cell suspension (e.g., 100 µL) is seeded into each well of Poly-D-lysine coated 96-well plate (The stock solution of poly-D-lysine is 100 μg / mL, diluted to 50 μg / mL by phosphate buffer, then directly added to 70 μL of blank 96-well plate. The plate is incubated overnight at 37 °C. After incubation, the incubation solution is discarded, and the plate is dried for use). Culture medium with 24 μg / mL (N-(7-Nitrobenz-2-Oxa-1,3-Diazol-4-yl)-1,2- Dihexadecanoyl-sn-Glycero-3-Phosphoethanolamine, Triethylammonium Salt) (NBD-PE) is prepared and filtered (e.g., with a 0.2 µm filter) before using. A volume of NBD-PE medium (e.g., 120 µL) is transferred to each well of the Poly-D-lysine coated 96-well cell culture plate seeded with HepG2 cells, and the plate is incubated for 24 hours at 37 °C with 95% humidity and 5% CO2atmosphere. After the incubation, the cell plate is moved out of the incubator. The working solutions are aspirated from the wells, and cells are fixed with 4% paraformaldehyde at room temperature for approximately 20 min. Then wells are washed twice with phosphate buffer (e.g., 100 μL), and Hoechst 33342 (e.g., 5 µM, 100 µL per well) is added into the plate. The plate is incubated at humidified, 37 °C, 5% CO2 atmosphere for 30 min. After 30 min of incubation at 37 °C, the dye is removed from the wells and the wells are washed twice with phosphate buffer (e.g., 100 μL for each wash). Phosphate buffer (e.g., 100 μL) is added to each well. The plate is scanned using a high-content imaging machine. Nine fields for each well are scanned and the fluorescence signals of NBD-PE and Hoechst 33342 are recorded simultaneously based on different florescence channels. The mean values of the fluorescence signals of 9 fields are output by the instrument for each well. The assays are performed in duplicate. The fluorescence of NBD-PE is used for the phospholipidosis calculation, while the fluorescence of Hoechst 33342 is used for the cell loss calculation. Data analysis is performed (e.g., using Microsoft Excel). A phospholipidosis Fold Change of a particular concentration of test compound can be calculated using the following equation: Fold Change = (Readtest compound / ReadVehicle) The Fold Change values are plotted against the concentration of the compound provided herein, or a pharmaceutically acceptable salt thereof, and the data are fit to a sigmoidal dose- response curve with a variable slope (e.g., using GraphPad Prism 8.0.2). The EC50value of the compound provided herein, or a pharmaceutically acceptable salt thereof, can be calculated from the curve using the following equation: Y = Bottom + (Top - Bottom) / (1+10^((LogEC50 - X)*HillSlope)) Where X is the log of the concentration of the compound provided herein, Bottom is the minimum Fold Change observed with the compound provided herein, and Top is the maximum Fold Change observed with the compound provided herein. A data point can be excluded if it is an outlier or an abnormal value due to cell death. Cell Loss is calculated using the following equation: Cell Loss (% Vehicle Control) = (Readtest compound / ReadVehicle Control)*100% The Cell Loss as a percentage of Vehicle Control is plotted against the concentration of test compound, and the data are fit to a sigmoidal dose-response curve with a variable slope (e.g., using GraphPad Prism 8.0.2). The IC50 of Cell Loss for the compound provided herein, or a pharmaceutically acceptable salt thereof, can be calculated from the curve using the following equation: Y = 100 / (1+ 10^((LogIC50 – X) × HillSlope)) Where X is the log of the concentration of the compound provided herein. Heterobifunctional degraders can, in some cases, induce the degradation of off-target proteins. For heterobifunctional degraders that utilize CRBN, common off-target proteins that can be degraded include GSPT1, IKZF1, IKZF2, IKZF3, and / or CK1α. This degradation is generally believed to be due to the E3 binding moiety of the heterobifunctional degrader facilitating ternary complex formation between the off-target protein and CRBN. GSPT1 is a translation termination factor, and CK1α is a kinase that is involved in many key cellular processes including cell cycle progression and chromosome segregation; these are both commonly essential genes, so undesired degradation of either or both can lead to nonspecific cytotoxicity. The IKZF proteins are zinc finger transcription factors that are involved with cell fate during hematopoiesis, and degradation of these proteins has been associated with hematotoxicity. See, e.g., Moreau, Kevin, et al. British Journal of Pharmacology 177.8 (2020): 1709-1718, doi: 10.1111 / bph.15014. In some embodiments, the compounds provided herein, or pharmaceutically acceptable salts thereof, can exhibit potent and selective induction of degradation of a BCL6 protein. In some embodiments, a compound provided herein, or a pharmaceutically acceptable salt thereof, or a pharmaceutically acceptable salt thereof, can selectively target a BCL6 protein for degradation over a second protein (e.g., GSPT1, IKZF1, IKZF2, IKZF3, CK1α, C6orf132, CAMP (cathelicidin antimicrobial peptide), CCNA2 (cyclin-A2), FSP1 (ferroptosis suppressor protein 1, also known as AIFM2), JCHAIN (immunoglobin J chain), NLRP7 (NACHT, LRR, PYD domains-containing protein 7), PTTG1 (securin), and / or TPX2 (targeting protein for Xklp2)). CAMP is an antimicrobial protein that is an integral part of the innate immune system, and it binds to bacterial lipopolysaccharides. CCNA2 controls both the G1 / S and the G2 / M transition phases of the cell cycle. FSP1 is an oxidoreductase that is an inhibitor of ferroptosis. JCHAIN links two monomer units of either IgM or IgA; the J chain-joined dimer is a nucleating unit of the IgM pentamer, and the J chain-joined dimer of IgA induces dimers or larger polymers. NLRP7 Inhibits CASP1 / caspase-1-dependent IL1B secretion. PTTG1 is key for chromosomal stability and negatively regulates TP53. TPX2 is required for the normal assembly of mitotic spindles. As used herein, “selective” or “selectively”, when referring to a compound provided herein, or a pharmaceutically acceptable salt thereof, in a protein degradation assay, indicates at least a 5-fold (e.g., at least a 10-fold, at least a 25-fold, at least a 50-fold, or at least a 100- fold) superior performance in the protein degradation assay for a specified protein with reference to a comparator protein in the assay. In some embodiments, the compounds provided herein can exhibit potency (e.g., nanomolar potency) against a BCL6 protein with minimal activity (e.g., single digit micromolar potency, for example, potency greater than 1 µM (e.g., greater than 3 µM, 5 µM, 10 µM, 20 µM, or 30 µM)) against a second protein. In some embodiments, a compound provided herein, or a pharmaceutically acceptable salt thereof, can exhibit potent degradation of a BCL6 protein and have minimal potency in degrading (e.g., as measured by Ymin, DC50, and / or Dmax values) a second protein (e.g., GSPT1, IKZF1, IKZF2, IKZF3, CK1α, C6orf132, CAMP, CCNA2, FSP1, JCHAIN, NLRP7, PTTG1, and / or TPX2). In some embodiments, a compound provided herein, or a pharmaceutically acceptable salt thereof, can exhibit greater induction of degradation of a BCL6 protein relative to induction of degradation (e.g., as measured by Ymin, DC50,and / or Dmaxvalues) of a second protein (e.g., GSPT1, IKZF1, IKZF2, IKZF3, CK1α, C6orf132, CAMP, CCNA2, FSP1, JCHAIN, NLRP7, PTTG1, and / or TPX2). In some embodiments, a compound provided herein, or a pharmaceutically acceptable salt thereof, can exhibit at least 2-fold, 3-fold, 5-fold, 10-fold, 25-fold, 50-fold, or 100-fold greater induction of degradation of a BCL6 protein relative to induction of degradation of a second protein. In some embodiments, a compound provided herein, or a pharmaceutically acceptable salt thereof, can exhibit up to 1000-fold greater induction of degradation of a BCL6 protein relative to induction of degradation of a second protein. In some embodiments, a compound provided herein, or a pharmaceutically acceptable salt thereof, can exhibit from about 2-fold to about 10-fold greater induction of degradation of a BCL6 protein relative to induction of degradation of a second protein (e.g., GSPT1, IKZF1, IKZF2, IKZF3, CK1α, C6orf132, CAMP, CCNA2, FSP1, JCHAIN, NLRP7, PTTG1, and / or TPX2) (e.g., as measured by Ymin, DC50,and / or Dmaxvalues). In some embodiments, a compound provided herein, or a pharmaceutically acceptable salt thereof, can exhibit from about 10-fold to about 100-fold greater induction of degradation of a BCL6 protein relative to induction of degradation of a second protein. In some embodiments, a compound provided herein, or a pharmaceutically acceptable salt thereof, can exhibit from about 100-fold to about 1000-fold greater induction of degradation of a BCL6 protein relative to induction of degradation of a second protein. In some embodiments, a compound provided herein, or a pharmaceutically acceptable salt thereof, can exhibit from about 1000-fold to about 10000-fold greater induction of degradation of a BCL6 protein relative to induction of degradation of a second protein. In some embodiments, the second protein is selected from the group consisting of GSPT1, IKZF1, IKZF2, IKZF3, CK1α, C6orf132, CAMP, CCNA2, FSP1, JCHAIN, NLRP7, PTTG1, and TPX2. In some embodiments, the second protein is selected from the group consisting of GSPT1, IKZF1, IKZF2, IKZF3, and CK1α. In some embodiments, the second protein is selected from the group consisting of C6orf132, CAMP, CCNA2, FSP1, JCHAIN, NLRP7, PTTG1, and TPX2. In some embodiments, the second protein is C6orf132. In some embodiments, the second protein is CAMP. In some embodiments, the second protein is CCNA2. In some embodiments, the second protein is FSP1. In some embodiments, the second protein is JCHAIN. In some embodiments, the second protein is NLRP7. In some embodiments, the second protein is PTTG1. In some embodiments, the second protein is TPX2. In some embodiments, the compounds provided herein can exhibit potency against a BCL6 protein with similar activity against a second protein (i.e., less than 2-fold greater activity against a BCL6 protein than against a second protein and no more than 2-fold greater activity against the second protein than against the BCL6 protein). In some embodiments, a compound provided herein, or a pharmaceutically acceptable salt thereof, can exhibit similar induction of degradation of a BCL6 protein relative to induction of degradation (e.g., as measured by Ymin, DC50, and / or Dmax values) of a second protein (i.e., less than 2-fold difference greater induction of degradation of a BCL6 protein than induction of degradation of a second protein and no more than 2-fold greater activity against the second protein than against a BCL6 protein) (e.g., GSPT1, IKZF1, IKZF2, IKZF3, CK1α, C6orf132, CAMP, CCNA2, FSP1, JCHAIN, NLRP7, PTTG1, and / or TPX2). In some embodiments, a compound provided herein, or a pharmaceutically acceptable salt thereof, can exhibit less than 2-fold greater induction of degradation of a BCL6 protein relative to induction of degradation of a second protein. In some embodiments, the second protein is selected from the group consisting of GSPT1, IKZF1, IKZF2, IKZF3, CK1α, C6orf132, CAMP, CCNA2, FSP1, JCHAIN, NLRP7, PTTG1, and TPX2. In some embodiments, the second protein is selected from the group consisting of GSPT1, IKZF1, IKZF2, IKZF3, and CK1α. In some embodiments, the second protein is selected from the group consisting of C6orf132, CAMP, CCNA2, FSP1, JCHAIN, NLRP7, PTTG1, and TPX2. In some embodiments, the second protein is C6orf132. In some embodiments, the second protein is CAMP. In some embodiments, the second protein is CCNA2. In some embodiments, the second protein is FSP1. In some embodiments, the second protein is JCHAIN. In some embodiments, the second protein is NLRP7. In some embodiments, the second protein is PTTG1. In some embodiments, the second protein is TPX2. In some embodiments, the compounds provided herein can exhibit potency against a BCL6 protein with minimal activity against a second protein (e.g., as measured by a proteomics assay, for example, a < 20% reduction in protein abundance as measured in the proteomics assay described herein). In some embodiments, a compound provided herein, or a pharmaceutically acceptable salt thereof, can exhibit potent degradation of a BCL6 protein and have minimal potency in degrading (e.g., as measured by abundance in a proteomic assay) a second protein (e.g., C6orf132, CAMP, CCNA2, FSP1, JCHAIN, NLRP7, PTTG, and / or TPX2) (e.g., as measured by abundance in a proteomic assay, for example, the proteomics assay as described herein). In some embodiments, a compound provided herein, or a pharmaceutically acceptable salt thereof, can exhibit greater induction of degradation of a BCL6 protein relative to induction of degradation (e.g., as measured by abundance in a proteomic assay, for example, the proteomics assay as described herein)of a second protein (e.g., C6orf132, CAMP, CCNA2, FSP1, JCHAIN, NLRP7, PTTG1, and / or TPX2). In some embodiments, a compound provided herein, or a pharmaceutically acceptable salt thereof, can exhibit at least 2-fold, 3-fold, 5-fold, 10-fold, 25-fold, 50-fold, or 100-fold greater induction of degradation of a BCL6 protein relative to induction of degradation of a second protein (e.g., C6orf132, CAMP, CCNA2, FSP1, JCHAIN, NLRP7, PTTG1, and / or TPX2) (e.g., as measured by abundance in a proteomic assay, for example, the proteomics assay as described herein). In some embodiments, a compound provided herein, or a pharmaceutically acceptable salt thereof, can exhibit up to 1000-fold greater induction of degradation of a BCL6 protein relative to induction of degradation of a second protein (e.g., C6orf132, CAMP, CCNA2, FSP1, JCHAIN, NLRP7, PTTG1, and / or TPX2) (e.g., as measured by abundance in a proteomic assay, for example, the proteomics assay as described herein). In some embodiments, a compound provided herein, or a pharmaceutically acceptable salt thereof, can exhibit from about 2-fold to about 10-fold greater induction of degradation of a BCL6 protein relative to induction of degradation of a second protein (e.g., C6orf132, CAMP, CCNA2, FSP1, JCHAIN, NLRP7, PTTG1, and / or TPX2) (e.g., as measured by abundance in a proteomic assay, for example, the proteomics assay as described herein). In some embodiments, a compound provided herein, or a pharmaceutically acceptable salt thereof, can exhibit from about 10-fold to about 100-fold greater induction of degradation of a BCL6 protein relative to induction of degradation of a second protein (e.g., C6orf132, CAMP, CCNA2, FSP1, JCHAIN, NLRP7, PTTG1, and / or TPX2) (e.g., as measured by abundance in a proteomic assay, for example, the proteomics assay as described herein). In some embodiments, a compound provided herein, or a pharmaceutically acceptable salt thereof, can exhibit from about 100-fold to about 1000-fold greater induction of degradation of a BCL6 protein relative to induction of degradation of a second protein (e.g., C6orf132, CAMP, CCNA2, FSP1, JCHAIN, NLRP7, PTTG1, and / or TPX2) (e.g., as measured by abundance in a proteomic assay, for example, the proteomics assay as described herein). In some embodiments, the second protein is selected from the group consisting of GSPT1, IKZF1, IKZF2, IKZF3, CK1α, C6orf132, CAMP, CCNA2, FSP1, JCHAIN, NLRP7, PTTG1, and TPX2. In some embodiments, the second protein is selected from the group consisting of GSPT1, IKZF1, IKZF2, IKZF3, and CK1α. In some embodiments, the second protein is selected from the group consisting of C6orf132, CAMP, CCNA2, FSP1, JCHAIN, NLRP7, PTTG1, and TPX2. In some embodiments, the second protein is C6orf132. In some embodiments, the second protein is CAMP. In some embodiments, the second protein is CCNA2. In some embodiments, the second protein is FSP1. In some embodiments, the second protein is JCHAIN. In some embodiments, the second protein is NLRP7. In some embodiments, the second protein is PTTG1. In some embodiments, the second protein is TPX2. In some embodiments, the compounds provided herein can exhibit potency against a BCL6 protein with minimal activity against any other detectable protein (e.g., as measured by a proteomics assay, for example, a < 20% reduction in protein abundance as measured in the proteomics assay described herein). In some embodiments, a compound provided herein, or a pharmaceutically acceptable salt thereof, can exhibit potent degradation of a BCL6 protein and have minimal potency in degrading (e.g., as measured by abundance in a proteomic assay, for example, the proteomics assay as described herein) any other detectable protein. In some embodiments, a compound provided herein, or a pharmaceutically acceptable salt thereof, can exhibit greater induction of degradation of a BCL6 protein relative to induction of degradation (e.g., as measured by abundance in a proteomic assay, for example, the proteomics assay as described herein) of any other detectable protein. In some embodiments, a compound provided herein, or a pharmaceutically acceptable salt thereof, can exhibit at least 2-fold, 3-fold, 5-fold, 10-fold, 25-fold, 50-fold, or 100-fold greater induction of degradation of a BCL6 protein relative to induction of degradation of any other detectable protein (e.g., as measured by abundance in a proteomic assay, for example, the proteomics assay as described herein). In some embodiments, a compound provided herein, or a pharmaceutically acceptable salt thereof, can exhibit up to 1000-fold greater induction of degradation of a BCL6 protein relative to induction of degradation of any other detectable protein (e.g., as measured by abundance in a proteomic assay, for example, the proteomics assay as described herein). In some embodiments, a compound provided herein, or a pharmaceutically acceptable salt thereof, can exhibit from about 2-fold to about 10-fold greater induction of degradation of a BCL6 protein relative to induction of degradation of any other detectable protein (e.g., as measured by abundance in a proteomic assay, for example, the proteomics assay as described herein). In some embodiments, a compound provided herein, or a pharmaceutically acceptable salt thereof, can exhibit from about 10-fold to about 100-fold greater induction of degradation of a BCL6 protein relative to induction of degradation of any other detectable protein (e.g., as measured by abundance in a proteomic assay, for example, the proteomics assay as described herein). In some embodiments, a compound provided herein, or a pharmaceutically acceptable salt thereof, can exhibit potent degradation of a BCL6 protein and have minimal potency in degrading one or more additional proteins as measured by abundance in a proteomic assay. An exemplary proteomic experiment follows. OCI-Ly1 (DSMZ: ACC 722) cells are incubated with 100 nM of a compound provided herein, or a pharmaceutically acceptable salt thereof, or dimethyl sulfoxide (DMSO), for six hours. The cells are then washed two times with phosphate buffered saline and collected. Cells are lysed to extract total proteins, and total proteins are prepared for mass spectrometry analysis according to the protocol for the EASYPEPTMMS Sample Prep Kit (Fisher Scientific). In brief, proteins are reduced with dithiothreitol, alkylated with iodoacetamide, and digested with Trypsin and LysC enzyme. The resulting peptides are labeled with TMTPRO™ 18plex reagents (Fisher Scientific) according to the manufacturer protocol. Labeled peptides from each sample are mixed together in equal volumes, and the peptide mixture is separated by basic reverse-phase chromatography. A total of 85 fractions are combined into 18 pooled fractions. The pooled fractions are dried with a centrivap and resuspended in 5% acetonitrile, 0.1% formic acid for mass spectrometry analysis. Peptide abundance is quantified by tandem mass spectrometry using a Vanquish Neo chromatography system (Fisher Scientific) and Orbitrap FUSION™ LUMOS™ mass spectrometer (Fisher Scientific). Briefly, two micrograms of total peptides are loaded on a two-centimeter C8 trap column followed by a 50-centimeter C18 column. Data-dependent acquisition is performed to obtain peptide sequence and abundance information. Peptide and protein abundances are determined using the PROTEOME DISCOVERER™ software and the Homo sapiens proteome database (TaxID 9606), and the results are filtered to FDR<0.01. Significance thresholds are set to p-value <0.001 and abundance fold-change < 50%. In some embodiments, a compound provided herein, or a pharmaceutically acceptable salt thereof, can degrade a BCL6 protein and minimally degrade one or more additional proteins as measured by abundance in a proteomic assay, for example, a proteomic assay that measures peptides on a proteome-wide basis following exposure of cells to a compound provided herein, or a pharmaceutically acceptable salt thereof, for a period of time. The abundance of measured peptides can be compared to a control experiment, and proteins increased or decreased following exposure to the compound provided herein, or a pharmaceutically acceptable salt thereof, can be identified. An exemplary protocol follows. Cells (e.g., OCI-Ly1 DSMZ: ACC 722) are incubated with a solution of 100 nM or 500 nM of a compound provided herein, or a pharmaceutically acceptable salt thereof, for 6 or 24 hours. After incubation, cells are washed two times with phosphate buffered saline, pelleted, and flash frozen in liquid nitrogen. Pellets are prepared for mass spectrometry analysis by using the Accelerome TMT 16-plex kit (Thermo Fisher #PIA50949) and an Accelerome (Thermo Fisher). Briefly, cells are lysed with lysis buffer containing universal nuclease and a cocktail of phosphatase and protease inhibitors (Thermo Fisher #78440). Protein extracts are digested with trypsin and LysC, reduced with dithiothreitol, and modified with iodoacetamide. Peptides are labeled with isobaric TMTpro reagent and combined. The combined, labeled peptides are separated by high-pH reverse phase fractionation using a C18 column (Phenomenex #00F- 4893-AN) on an Agilent 1260 Infinity II HPLC. A total of 85 fractions are combined into 18 pooled fractions. The pooled fractions are dried with a centrivap and resuspended in 0.1% formic acid, 5% acetonitrile for analysis on an Orbitrap Ascend mass spectrometer (Thermo Fisher). Peptides are resolved using a 90-minute reverse phase gradient and a 50 cm C18 column (Thermo Fisher #ES903). A data-dependent SPS-MS3 analysis method is used with the default settings (e.g., MS1 scan with 120000 orbitrap resolution, Scan Range of 400-1600 m / z, and RF Lens of 60%; MS2 scan with CID fragmentation, 30% Collision Energy, Ion Trap detector, Turbo Scan Rate, and 45 ms injection time; MS3 scan with HCD fragmentation, 55% Collision Energy, Orbitrap detector, 45000 resolution, TurboTMT off, and 200 ms injection time). Real-time search is enabled with the Homo sapiens proteome database (Uniprot 9606, downloaded 7 / 10 / 23), Static Modifications of “Carbamidomethyl” and “TMTpro16plex”, and Variable Modification “Oxidation M”. Raw files are processed to identify and quantify proteins using Proteome Discoverer version 3.0. Data are searched against the human proteome (above). Processing method “PWF_Tribrid_TMTpro_Quan_SPS_MS3_SequestFT_Percolator” and Consensus method “CWF_Comprehensive_Enhanced Annotation_Reporter_Quan_MS3” are used to generate protein quantitation values. The Sequest HT node included dynamic modifications of oxidation on Met, phosphorylation on Ser, Thr, and Tyr, and static modifications of TMTpro on Lys and peptide N-terminus and Carbamidomethyl on Cys. As used herein, “determining BCL6 expression status,” means assessing whether or not BCL6 is expressed, e.g., at the mRNA or protein level. In some embodiments, the assessment includes the level of BCL6 expression (e.g., BCL6 expression above or below a threshold value). BCL6 expression status can be assessed by a variety of methods (e.g., measuring protein levels, mRNA levels, or both) and can be assessed quantitatively or qualitatively, e.g., using a scale or threshold accepted by, e.g., a regulatory agency or by a pathologist. In some embodiments, the assessment includes consulting the medical record of a subject. In some embodiments, the BCL6 expression status is positive (e.g., the sample from the subject is positive for BCL6 expression). In some embodiments the BCL6 expression status is not positive for BCL6 expression (e.g., the sample from the subject is negative or indeterminate, for example, BCL6 expression is below a threshold value or below the lower limit of detection for a particular assay). In some embodiments, a BCL6 expression status can be determined for a sample from a subject. In some embodiments, the BCL6 expression status can be determined by expression profiling (e.g., mRNA expression profiling) (e.g., of a sample of the cancer or from a blood sample). In some embodiments, the BCL6 expression status can be determined by an mRNA- based test, such as RNA sequencing (RNA-seq), reverse transcription polymerase chain reaction (RT-PCR), digital PCR (dPCR), or in-situ hybridization (ISH). In some embodiments, the BCL6 expression status can be determined by an IHC test, using any appropriate IHC method and reagents. For example, a pathologist or an automated system (e.g., the BOND RX system (Leica), the BOND-PRIME system (Leica), the AutoStainer Link 48 system (Agilent), the AutoStainer PLUS system (Agilent), the Dako Omnis system (Agilent), the BenchMark ULTRA system (Roche), or the BenchMark ULTRA PLUS system (Roche)) can determine that a sample of the cancer (e.g., a biopsy sample) from the subject subjected to IHC with an appropriate BCL6 antibody is positive for BCL6 expression. As another example, an IHC test can result in an IHC score of 0, 1, 2, or 3; in some such embodiments, a positive BCL6 expression status can be indicated by a score of 1, 2, or 3 (e.g., 2 or 3) (e.g., as determined by a pathologist or an automated system). As yet another example, an IHC test may result in a percent nuclear positivity score from 0% to 100%; in some such embodiments, a positive BCL6 expression status can be indicated by a percent nuclear positivity score of greater than or equal to 1% (e.g., greater than or equal to 5%, greater than or equal to 10%, greater than or equal to 15%, or greater than or equal to 20%). In some embodiments, a positive BCL6 expression status can be indicated by a percent nuclear positivity score of greater than or equal to 30% (e.g., greater than or equal to 35%, greater than or equal to 40%, or greater than or equal to 50%) (e.g., as determined by a pathologist or an automated system). See, e.g., Hans, Christine P., et al. Blood 103.1 (2004): 275-282, doi: 10.1182 / blood-2003-05-1545. In some such embodiments, the sample from the subject can have a percent nuclear positivity score of greater than or equal to 75% (e.g., greater than or equal to 80%, greater than or equal to 90%, or greater than or equal to 95%) (e.g., as determined by a pathologist or an automated system). As another example, an IHC test can result in an H-score from 0 to 300; in some such embodiments, a positive BCL6 expression status can be indicated by an H-score of greater than or equal to 10 (e.g., greater than or equal to 30, greater than or equal to 50, greater than or equal to 60, greater than or equal to 75, greater than or equal to 100, greater than or equal to 150, or greater than or equal to 200). In some embodiments, an H-score is calculated as 3 x percentage of strongly staining nuclei + 2 x percentage of moderately staining nuclei + percentage of weakly staining nuclei. Non-limiting examples of antibodies suitable for an IHC test of BCL6 expression include clone PG-B6p (e.g., Dako / Agilent product number IR625), clone GI191E / A8 (e.g., Roche / Ventana product number 760-4241), clone LN22 (e.g., Lecia Biosystems product number PA0204), clone GI191E / A8 (e.g., Sigma / Cell Marque product number 227M-98), and clone EP278 (e.g., Sigma / Cell Marque product number 227R-27). Provided herein is a method of treating a cancer in a subject in need thereof, the method comprising administering to the subject a therapeutically effective amount of a compound provided herein, or a pharmaceutically acceptable salt thereof, or a pharmaceutical composition comprising a compound provided herein, or a pharmaceutically acceptable salt thereof. In some embodiments, the cancer in the subject is positive for BCL6 expression. In some embodiments, the cancer in the subject is negative for BCL6 expression. Accordingly, also provided herein is a method of treating cancer in a subject in need thereof, the method comprising (a) determining the BCL6 expression status of the cancer (e.g., by performing an assay or a test, or consulting the subject’s medical record); and (b) administering to the subject a therapeutically effective amount of a compound provided herein, or a pharmaceutically acceptable salt thereof, or a pharmaceutical composition comprising a compound provided herein, or a pharmaceutically acceptable salt thereof. Also provided herein is a method of treating cancer in a subject in need thereof, the method comprising: (a) determining that the cancer in the subject is positive for BCL6 expression (e.g., determining that the cancer is positive for BCL6 expression by an IHC test); and (b) administering to the subject a therapeutically effective amount of a compound provided herein, or a pharmaceutically acceptable salt thereof, or a pharmaceutical composition comprising a compound provided herein, or a pharmaceutically acceptable salt thereof. Also provided herein is a method of treating cancer in a subject in need thereof, the method comprising: (a) determining the BCL6 expression status of the cancer; and (b) administering to the subject a therapeutically effective amount of a compound provided herein, or a pharmaceutically acceptable salt thereof, or a pharmaceutical composition comprising a compound provided herein, or a pharmaceutically acceptable salt thereof. In some such embodiments, the cancer in the subject is positive for BCL6 expression. In other such embodiments, the cancer in the subject is not positive for BCL6 expression. Also provided herein is a method of treating cancer, the method comprising administering to a subject determined to have a cancer that is positive for BCL6 expression (e.g., a subject determined to have a cancer that is positive for BCL6 expression by an IHC test) a therapeutically effective amount of a compound provided herein, or a pharmaceutically acceptable salt thereof, or a pharmaceutical composition comprising a compound provided herein, or a pharmaceutically acceptable salt thereof. Also provided herein is a method of treating cancer, the method comprising administering to a subject having a cancer previously tested for BCL6 expression status (e.g., a subject having a cancer previously tested for BCL6 expression by an IHC test) a therapeutically effective amount of a compound provided herein, or a pharmaceutically acceptable salt thereof, or a pharmaceutical composition comprising a compound provided herein, or a pharmaceutically acceptable salt thereof. In some such embodiments, the cancer in the subject is positive for BCL6 expression. In other such embodiments, the cancer in the subject is not positive for BCL6 expression. Also provided herein is a method of treating cancer, the method comprising administering to a subject who has a record (e.g., a medical record) that indicates that the cancer in the subject is positive for BCL6 expression (e.g., a subject previously identified as having a cancer that is positive for BCL6 expression by an IHC test) a therapeutically effective amount of a compound provided herein, or a pharmaceutically acceptable salt thereof, or a pharmaceutical composition comprising a compound provided herein, or a pharmaceutically acceptable salt thereof. Also provided herein is a method of treating cancer, the method comprising administering to a subject who has a record (e.g., a medical record) that indicates that the cancer in the subject was previously tested for BCL6 expression (e.g., a subject identified as having a cancer that was previously tested for BCL6 expression by an IHC test) a therapeutically effective amount of a compound provided herein, or a pharmaceutically acceptable salt thereof, or a pharmaceutical composition comprising a compound provided herein, or a pharmaceutically acceptable salt thereof. In some such embodiments, the cancer in the subject is positive for BCL6 expression. In other such embodiments, the cancer in the subject is not positive for BCL6 expression. Also provided herein is a method of treating cancer, the method comprising administering a therapeutically effective amount of a compound provided herein, or a pharmaceutically acceptable salt thereof, or a pharmaceutical composition comprising a compound provided herein, or a pharmaceutically acceptable salt thereof, to a subject determined to have a cancer that is positive for BCL6 expression (e.g., a cancer that is positive for BCL6 expression by an IHC test). Also provided herein is a method of treating cancer, the method comprising administering a therapeutically effective amount of a compound provided herein, or a pharmaceutically acceptable salt thereof, or a pharmaceutical composition comprising a compound provided herein, or a pharmaceutically acceptable salt thereof, to a subject determined to have a cancer previously tested for BCL6 expression (e.g., a cancer previously tested for BCL6 expression by an IHC test). In some such embodiments, the cancer in the subject is positive for BCL6 expression. In other such embodiments, the cancer in the subject is not positive for BCL6 expression. In some embodiments, provided herein is a method of treating cancer in a subject that includes performing an assay on a sample (e.g., a tumor sample) obtained from the subject to determine that the cancer in the subject is positive for BCL6 expression, and administering a therapeutically effective amount of a compound provided herein, or a pharmaceutically acceptable salt thereof, or a pharmaceutical composition comprising a compound provided herein, or a pharmaceutically acceptable salt thereof, to the subject having a cancer determined to be positive for BCL6 expression. In some embodiments, provided herein is a method of treating cancer in a subject that includes performing an assay on a sample (e.g., a tumor sample) obtained from the subject to determine the BCL6 expression status of the cancer, and administering a therapeutically effective amount of a compound provided herein, or a pharmaceutically acceptable salt thereof, or a pharmaceutical composition comprising a compound provided herein, or a pharmaceutically acceptable salt thereof, to the subject. In some such embodiments, the cancer in the subject is positive for BCL6 expression. In other such embodiments, the cancer in the subject is not positive for BCL6 expression. In some embodiments of any of these methods, the BCL6 expression status of the cancer is determined after administration of at least one dose (e.g., two doses, three doses, four doses, five doses, or more) of a compound provided herein, or a pharmaceutically acceptable salt thereof, or a pharmaceutical composition comprising a compound provided herein, or a pharmaceutically acceptable salt thereof, to the subject (e.g., the BCL6 expression status of the cancer is determined via a biopsy or a blood sample). In some embodiments, the subject is suspected of having a cancer that is positive for BCL6 expression, is presenting with one or more symptoms of a cancer expressing BCL6, or has an elevated risk of developing a cancer that is positive for BCL6 expression. In some embodiments, the subject is treatment naïve with respect to the cancer. In some embodiments, the subject has received one or more lines of previous therapy for the cancer. In some embodiments of any of these methods, the compound provided herein, or a pharmaceutically acceptable salt thereof, or a pharmaceutical composition comprising a compound provided herein, or a pharmaceutically acceptable salt thereof, is administered to the subject as a monotherapy. Some embodiments of these methods further include administering to the subject an additional therapy or therapeutic agent. In some embodiments, the cancer is a large B cell lymphoma (LBCL) (e.g., diffuse large B-cell lymphoma not otherwise specified (DLBCL-NOS), diffuse large B-cell lymphoma / high grade B cell lymphoma (HGBCL) (e.g., HGBCL with MYC and / or BCL2 rearrangements (HGBCL-MYC / BCL-2)), primary LBCL of immune-privileged sites, primary mediastinal LBCL, or HBGCL-NOS). In some embodiments, the LBCL is positive for BCL6 expression as determined by an IHC test (e.g., indicated by a percent nuclear positivity score of greater than or equal to 30% in an IHC test). In some embodiments, the cancer is DLBCL- NOS; in some such embodiments, the DLBCL-NOS is positive for BCL6 expression as determined by an IHC test (e.g., indicated by a percent nuclear positivity score of greater than or equal to 30% in an IHC test). In some embodiments, the cancer is HGBCL-MYC / BCL-2 or HGBCL-NOS; in some such embodiments, the HGBCL-MYC / BCL-2 or HGBCL-NOS is positive for BCL6 expression as determined by an IHC test (e.g., indicated by a percent nuclear positivity score of greater than or equal to 30% in an IHC test). In some embodiments, the cancer is primary LBCL of immune-privileged sites; in some such embodiments, the primary LBCL of immune-privileged sites is positive for BCL6 expression as determined by an IHC test (e.g., indicated by a percent nuclear positivity score of greater than or equal to 30% in an IHC test). In some embodiments, the cancer is primary mediastinal LBCL; in some such embodiments, the primary mediastinal LBCL is positive for BCL6 expression as determined by an IHC test (e.g., indicated by a percent nuclear positivity score of greater than or equal to 30% in an IHC test). In some embodiments, the cancer is a transformed indolent B cell lymphoma. In some embodiments, the transformed indolent B cell lymphoma is positive for BCL6 expression as determined by an IHC test (e.g., indicated by a percent nuclear positivity score of greater than or equal to 1% in an IHC test; e.g., a percent nuclear positivity score of greater than or equal to 30% in an IHC test). In some embodiments, the cancer is FL. In some embodiments, the FL is positive for BCL6 expression as determined by an IHC test (e.g., indicated by a percent nuclear positivity score of greater than or equal to 1% in an IHC test; e.g., a percent nuclear positivity score of greater than or equal to 30% in an IHC test). In some embodiments, the cancer is BL. In some embodiments, the BL is positive for BCL6 expression as determined by an IHC test (e.g., indicated by a percent nuclear positivity score of greater than or equal to 1% in an IHC test; e.g., a percent nuclear positivity score of greater than or equal to 30% in an IHC test). In some embodiments, the cancer is NLPHL. In some embodiments, the NLPHL is positive for BCL6 expression as determined by an IHC test (e.g., indicated by a percent nuclear positivity score of greater than or equal to 1% in an IHC test; e.g., a percent nuclear positivity score of greater than or equal to 30% in an IHC test). In some embodiments, the cancer is a peripheral T-cell lymphoma (PTCL) (e.g., anaplastic large cell lymphoma (ALCL) (e.g., ALK-positive anaplastic large cell lymphoma, or ALK-negative anaplastic large cell lymphoma), nodal T follicular helper cell lymphoma (e.g., nodal T follicular helper cell lymphoma angioimmunoblastic type (also known as angioimmunoblastic T-cell lymphoma (AITL) or follicular helper T-cell lymphoma, angioimmunoblastic type), nodal T follicular helper cell lymphoma follicular type (also known as follicular helper T-cell lymphoma, follicular type), or nodal T follicular helper cell lymphoma NOS (also known as follicular helper T-cell lymphoma, NOS))) or a primary cutaneous T-cell lymphoid proliferation or lymphoma (cutaneous T-cell lymphoma (CTCL)) (e.g., primary cutaneous CD4-positive small or medium T-cell lymphoproliferative disorder, mycosis fungoides, Sezary syndrome, or primary cutaneous gamma-delta T-cell lymphoma). In some embodiments, the PTCL or CTCL is positive for BCL6 expression as determined by an IHC test (e.g., indicated by a percent nuclear positivity score of greater than or equal to 1% in an IHC test; e.g., a percent nuclear positivity score of greater than or equal to 30% in an IHC test). In some embodiments, the cancer is a nodal T follicular helper cell lymphoma (e.g., nodal T follicular helper cell lymphoma angioimmunoblastic type (also known as angioimmunoblastic T-cell lymphoma (AITL) or follicular helper T-cell lymphoma, angioimmunoblastic type), nodal T follicular helper cell lymphoma follicular type (also known as follicular helper T-cell lymphoma, follicular type), or nodal T follicular helper cell lymphoma NOS (also known as follicular helper T-cell lymphoma, NOS)). In some such embodiments, the nodal T follicular helper cell lymphoma (e.g., nodal T follicular helper cell lymphoma angioimmunoblastic type (also known as angioimmunoblastic T-cell lymphoma (AITL) or follicular helper T-cell lymphoma, angioimmunoblastic type), nodal T follicular helper cell lymphoma follicular type (also known as follicular helper T-cell lymphoma, follicular type), or nodal T follicular helper cell lymphoma NOS (also known as follicular helper T-cell lymphoma, NOS)) is positive for BCL6 expression as determined by an IHC test (e.g., indicated by a percent nuclear positivity score of greater than or equal to 1% in an IHC test; e.g., a percent nuclear positivity score of greater than or equal to 30% in an IHC test). In some embodiments, the cancer is nodal T follicular helper cell lymphoma follicular type. In some such embodiments, the nodal T follicular helper cell lymphoma follicular type is positive for BCL6 expression as determined by an IHC test (e.g., indicated by a percent nuclear positivity score of greater than or equal to 1% in an IHC test; e.g., a percent nuclear positivity score of greater than or equal to 30% in an IHC test). In some embodiments, the cancer is nodal T follicular helper cell lymphoma angioimmunoblastic type. In some such embodiments, the nodal T follicular helper cell lymphoma angioimmunoblastic type is positive for BCL6 expression as determined by an IHC test (e.g., indicated by a percent nuclear positivity score of greater than or equal to 1% in an IHC test; e.g., a percent nuclear positivity score of greater than or equal to 30% in an IHC test). In some embodiments, the cancer is anaplastic large cell lymphoma (ALCL) (e.g., ALK-positive anaplastic large cell lymphoma, or ALK-negative anaplastic large cell lymphoma). In some such embodiments, the anaplastic large cell lymphoma (ALCL) (e.g., ALK-positive anaplastic large cell lymphoma, or ALK-negative anaplastic large cell lymphoma) is positive for BCL6 expression as determined by an IHC test (e.g., indicated by a percent nuclear positivity score of greater than or equal to 1% in an IHC test; e.g., a percent nuclear positivity score of greater than or equal to 30% in an IHC test). In some embodiments, the cancer is nodal T follicular helper cell lymphoma NOS. In some such embodiments, the nodal T follicular helper cell lymphoma NOS is positive for BCL6 expression as determined by an IHC test (e.g., indicated by a percent nuclear positivity score of greater than or equal to 1% in an IHC test; e.g., a percent nuclear positivity score of greater than or equal to 30% in an IHC test). In some embodiments, the cancer is a primary cutaneous T-cell lymphoid proliferation or lymphoma (cutaneous T-cell lymphoma (CTCL)) (e.g., primary cutaneous CD4-positive small or medium T-cell lymphoproliferative disorder, mycosis fungoides, Sezary syndrome, or primary cutaneous gamma-delta T-cell lymphoma). In some such embodiments, the primary cutaneous T-cell lymphoid proliferation or lymphoma (cutaneous T-cell lymphoma (CTCL)) (e.g., primary cutaneous CD4-positive small or medium T-cell lymphoproliferative disorder, mycosis fungoides, Sezary syndrome, or primary cutaneous gamma-delta T-cell lymphoma) is positive for BCL6 expression as determined by an IHC test (e.g., indicated by a percent nuclear positivity score of greater than or equal to 1% in an IHC test; e.g., a percent nuclear positivity score of greater than or equal to 30% in an IHC test). In some embodiments, the cancer is mycosis fungoides. In some such embodiments, the mycosis fungoides is positive for BCL6 expression as determined by an IHC test (e.g., indicated by a percent nuclear positivity score of greater than or equal to 1% in an IHC test; e.g., a percent nuclear positivity score of greater than or equal to 30% in an IHC test). In some embodiments, the cancer is primary cutaneous CD4-positive small or medium T-cell lymphoproliferative disorder. In some such embodiments, the primary cutaneous CD4-positive small or medium T-cell lymphoproliferative disorder is positive for BCL6 expression as determined by an IHC test (e.g., indicated by a percent nuclear positivity score of greater than or equal to 1% in an IHC test; e.g., a percent nuclear positivity score of greater than or equal to 30% in an IHC test). In some embodiments, the cancer is mycosis fungoides. In some such embodiments, the mycosis fungoides is positive for BCL6 expression as determined by an IHC test (e.g., indicated by a percent nuclear positivity score of greater than or equal to 1% in an IHC test; e.g., a percent nuclear positivity score of greater than or equal to 30% in an IHC test). In some embodiments, the cancer is primary cutaneous gamma-delta T-cell lymphoma. In some such embodiments, the primary cutaneous gamma-delta T-cell lymphoma is positive for BCL6 expression as determined by an IHC test (e.g., indicated by a percent nuclear positivity score of greater than or equal to 1% in an IHC test; e.g., a percent nuclear positivity score of greater than or equal to 30% in an IHC test). In some embodiments, the cancer is Sezary syndrome. In some such embodiments, the Sezary syndrome is positive for BCL6 expression as determined by an IHC test (e.g., indicated by a percent nuclear positivity score of greater than or equal to 1% in an IHC test; e.g., a percent nuclear positivity score of greater than or equal to 30% in an IHC test). In some cases, treatment of a cancer or a model of a cancer (e.g., a PDX or CDX model) with a compound provided herein, or a pharmaceutically acceptable salt thereof, or a pharmaceutical composition comprising a compound provided herein, or a pharmaceutically acceptable salt thereof, can result in a regression (e.g., greater than or equal to 50% regression) of the cancer or the model of the cancer. In some cases, treatment of a cancer or a model of a cancer (e.g., a PDX or CDX model) with a compound provided herein, or a pharmaceutically acceptable salt thereof, or a pharmaceutical composition comprising a compound provided herein, or a pharmaceutically acceptable salt thereof, as a monotherapy can result in a regression (e.g., greater than or equal to 50% regression) of the cancer or the model of the cancer. In some such embodiments, the PDX model is positive for BCL6 expression as determined by an IHC test (e.g., indicated by a percent nuclear positivity score of greater than or equal to 30% in an IHC test). In some embodiments, the PDX model is positive for MYC expression as determined by an IHC test (e.g., indicated by a percent nuclear positivity score of greater than or equal to 30% in an IHC test). In some such embodiments, the PDX model is positive for BCL6 expression as determined by an IHC test (e.g., indicated by a percent nuclear positivity score of greater than or equal to 30% in an IHC test) and positive for MYC expression as determined by an IHC test (e.g., indicated by a percent nuclear positivity score of greater than or equal to 30% in an IHC test). Provided herein is use of a compound provided herein, or a pharmaceutically acceptable salt thereof, or a pharmaceutical composition thereof, for the treatment of cancer, for example, any of the cancers provided herein. Also provided herein is use of a compound provided herein, or a pharmaceutically acceptable salt thereof, or a pharmaceutical composition thereof, for the treatment of a cancer that is positive for BCL6 expression (e.g., as determined by an IHC test). Provided herein is use of a compound provided herein, or a pharmaceutically acceptable salt thereof, or a pharmaceutical composition thereof, as a medicament for the treatment of cancer, for example, any of the cancers provided herein. Also provided herein is use of a compound provided herein, or a pharmaceutically acceptable salt thereof, or a pharmaceutical composition thereof, as a medicament for the treatment of a cancer that is positive for BCL6 expression (e.g., as determined by an IHC test). Provided herein is use of a compound provided herein, or a pharmaceutically acceptable salt thereof, in the manufacture of a medicament for the treatment of cancer, for example, any of the cancers provided herein. Also provided herein is use of a compound provided herein, or a pharmaceutically acceptable salt thereof, in the manufacture of a medicament for the treatment of a cancer that is positive for BCL6 expression (e.g., as determined by an IHC test). Provided herein is a compound provided herein, or a pharmaceutically acceptable salt thereof, or a pharmaceutical composition thereof, for use as a medicament. Also provided herein is a compound provided herein, or a pharmaceutically acceptable salt thereof, or a pharmaceutical composition thereof, for use as a medicament for the treatment of cancer, for example, any of the cancers provided herein. Also provided herein is a compound provided herein, or a pharmaceutically acceptable salt thereof, or a pharmaceutical composition thereof, for use as a medicament in the treatment of a cancer that is positive for BCL6 expression (e.g., as determined by an IHC test). Provided herein is a compound provided herein, or a pharmaceutically acceptable salt thereof, or a pharmaceutical composition thereof, for use in treating a cancer, for example, any of the cancers provided herein. Also provided is a compound provided herein, or a pharmaceutically acceptable salt thereof, or a pharmaceutical composition thereof, for use in treating a cancer that is positive for BCL6 expression in a subject identified or diagnosed as having a cancer that is positive for BCL6 expression through a step of performing a test (e.g., an IHC test) on a sample (e.g., a tumor sample) obtained from the subject to determine whether the cancer in the subject that is positive for BCL6 expression (e.g., as determined by an IHC test). As used herein, treatment of a cancer can include treatment of a primary tumor (i.e., non-metastatic cancer) (e.g., as first, second, third, or later line of therapy, including, but not limited to, the relapsed / refractory setting), treatment of a metastatic (or secondary) tumor, neoadjuvant therapy (e.g., before treatment with an additional therapy or therapeutic agent, such as surgery, radiation, chemotherapy, or a line of therapy), adjuvant therapy (e.g., following treatment with an additional therapy or therapeutic agent, such as surgery, radiation, chemotherapy, or a line of therapy), or maintenance therapy (e.g., treatment following response to an additional therapy or therapeutic agent, such as surgery, radiation, chemotherapy, or a line of therapy). In some embodiments, a compound provided herein, or a pharmaceutically acceptable salt thereof is used in the treatment of a primary tumor. In some embodiments, the subject is treatment naïve with respect to the cancer. In some embodiments, the subject has received one or more lines of therapy for the cancer. In some embodiments, the subject has received chemotherapy, cell-based therapy (e.g., adoptive cell therapy (e.g., CAR T therapy, cytokine- induced killer cells (CIKs), natural killer cells (e.g., CAR-modified NK cells)) or antibody- armed cell therapy), or both. In some embodiments, the subject has received R-CHOP, G- CHOP, R-EPOCH, CVP, CVAD, R2, R-CODOX-M, R-IVAC, DA-EPOCH-R, cell-based therapy, or two or more thereof. In some embodiments, the subject has received a rituximab- containing regimen. In some embodiments, the subject has received an obinutuzumab- containing regimen. In some embodiments, the subject has received a mosunetuzumab- containing regimen. In some embodiments, the subject has received an epcoritamab-containing regimen. In some embodiments, the compound provided herein, or a pharmaceutically acceptable salt thereof is used in the treatment of a subject who has received one or more lines of systemic therapy for the cancer. In some embodiments, the compound provided herein, or a pharmaceutically acceptable salt thereof is used in the treatment of a subject who has received two or more lines of systemic therapy for the cancer. In some embodiments, a compound provided herein, or a pharmaceutically acceptable salt thereof is used in the treatment of a metastatic tumor. In some embodiments, the subject is treatment naïve with respect to the metastatic tumor. In some embodiments, the subject has received one or more lines of therapy for the secondary tumor. In some embodiments, the subject has received chemotherapy, cell-based therapy (e.g., adoptive cell therapy (e.g., CAR T therapy, cytokine-induced killer cells (CIKs), natural killer cells (e.g., CAR-modified NK cells)) or antibody-armed cell therapy), or both. In some embodiments, the subject has received R-CHOP, G-CHOP, R-EPOCH, CVP, CVAD, R2, R-CODOX-M, R-IVAC, DA-EPOCH-R, cell-based therapy, or two or more thereof. In some embodiments, the subject has received a rituximab-containing regimen. In some embodiments, the subject has received an obinutuzumab-containing regimen. In some embodiments, the subject has received a mosunetuzumab-containing regimen. In some embodiments, the subject has received an epcoritamab-containing regimen. In some embodiments, the compound provided herein, or a pharmaceutically acceptable salt thereof is used in the treatment of a subject who has received one or more lines of systemic therapy for the cancer. In some embodiments, the compound provided herein, or a pharmaceutically acceptable salt thereof is used in the treatment of a subject who has received two or more lines of systemic therapy for the cancer. In some embodiments, a compound provided herein, or a pharmaceutically acceptable salt thereof is used as neoadjuvant therapy. In some embodiments, the neoadjuvant therapy precedes surgery (e.g., surgical resection, such as partial surgical resection or complete, total, or full surgical resection). In some embodiments, the neoadjuvant therapy precedes radiation therapy. In some embodiments, the neoadjuvant therapy precedes chemotherapy. In some embodiments, a compound provided herein, or a pharmaceutically acceptable salt thereof is an adjuvant therapy. In some embodiments, the subject has received chemotherapy, cell-based therapy (e.g., adoptive cell therapy (e.g., CAR T therapy, cytokine- induced killer cells (CIKs), natural killer cells (e.g., CAR-modified NK cells)) or antibody- armed cell therapy), or both. In some embodiments, the subject has received R-CHOP, G- CHOP, R-EPOCH, CVP, CVAD, R2, R-CODOX-M, R-IVAC, DA-EPOCH-R, cell-based therapy, or two or more thereof. In some embodiments, the subject has received a rituximab- containing regimen. In some embodiments, the subject has received an obinutuzumab- containing regimen. In some embodiments, the subject has received a mosunetuzumab- containing regimen. In some embodiments, the subject has received an epcoritamab-containing regimen. In some embodiments, the compound provided herein, or a pharmaceutically acceptable salt thereof is used in the treatment of a subject who has received one or more lines of systemic therapy for the cancer. In some embodiments, the compound provided herein, or a pharmaceutically acceptable salt thereof is used in the treatment of a subject who has received two or more lines of systemic therapy for the cancer. In some embodiments, the adjuvant therapy follows surgery (e.g., surgical resection, such as partial surgical resection or complete, total, or full surgical resection). In some embodiments, the adjuvant therapy follows radiation therapy. In some embodiments, the adjuvant therapy follows chemotherapy. In some embodiments, a compound provided herein, or a pharmaceutically acceptable salt thereof is a maintenance therapy. In some embodiments, the subject has received chemotherapy, cell-based therapy (e.g., adoptive cell therapy (e.g., CAR T therapy, cytokine- induced killer cells (CIKs), natural killer cells (e.g., CAR-modified NK cells)) or antibody- armed cell therapy), a stem cell transplant, or a combination thereof. In some embodiments, the subject has received R-CHOP, G-CHOP, R-EPOCH, CVP, CVAD, R2, R-CODOX-M, R- IVAC, DA-EPOCH-R, cell-based therapy, or two or more thereof. In some embodiments, the subject has received a rituximab-containing regimen. In some embodiments, the subject has received an obinutuzumab-containing regimen. In some embodiments, the subject has received a mosunetuzumab-containing regimen. In some embodiments, the subject has received an epcoritamab-containing regimen. In some embodiments, the subject has received a stem cell transplant. In some embodiments, the subject has received a cell-based therapy (e.g., CAR T therapy). In some embodiments, the compound provided herein, or a pharmaceutically acceptable salt thereof is used in the treatment of a subject who has received one or more lines of systemic therapy for the cancer. In some embodiments, the compound provided herein, or a pharmaceutically acceptable salt thereof is used in the treatment of a subject who has received two or more lines of systemic therapy for the cancer. As used herein, “monotherapy”, when referring to a compound provided herein, or a pharmaceutically acceptable salt thereof, means that the compound provided herein, or a pharmaceutically acceptable salt thereof, is the only therapeutic agent or therapy (e.g., anticancer agent or therapy) administered to the subject during the treatment cycle (e.g., no additional targeted therapeutics, anticancer agents, chemotherapeutics, or checkpoint inhibitors are administered to the subject during the treatment cycle). As a person of ordinary skill in the art would understand, monotherapy does not exclude the co-administration of medicaments for the treatment of side effects or general symptoms associated with the cancer or treatment, such as pain, rash, edema, photosensitivity, pruritis, skin discoloration, hair brittleness, hair loss, brittle nails, cracked nails, discolored nails, swollen cuticles, fatigue, weight loss, general malaise, shortness of breath, infection, anemia, or gastrointestinal symptoms, including nausea, diarrhea, and lack of appetite. As used herein, “the subject has received one or more lines of therapy for the cancer” means that the subject has been previously administered one or more therapeutic agents or therapies (e.g., anticancer agent or therapy) for the cancer other than a compound provided herein, or a pharmaceutically acceptable salt thereof, during a prior treatment cycle. In some embodiments, the subject cannot tolerate the one or more therapeutic agents or therapies previously administered for the cancer. In some embodiments, the subject did not respond to the one or more therapeutic agents or therapies previously administered for the cancer. In some embodiments, the subject did not adequately respond to one or more therapeutic agents or therapies previously administered for the cancer. In some embodiments, the subject has stopped responding to the one or more therapeutic agents or therapies previously administered for the cancer. In some embodiments, a lack of response, an inadequate response, or a discontinued response can be determined by objective criteria (e.g., tumor volume, or by criteria such as RECIST 1.1, the Lugano 2014 criteria (Cheson, Bruce D., et al. Journal of Clinical Oncology 32.27 (2014): 3059-3067; doi: 10.1200 / JCO.2013.54.8800) or the Global Response Criteria (Olsen, Elise A., et al. Blood, The Journal of the American Society of Hematology 140.5 (2022): 419-437; doi: 10.1182 / blood.2021012057)). In some embodiments, a lack of response, an inadequate response, or a discontinued response can be determined by the subject’s physician. As used herein, “the subject is treatment naïve with respect to the cancer” means that the subject has not been previously administered one or more therapeutic agents or therapies for the cancer. For any of the solid tumors described herein, the solid tumor can be primary tumors or metastatic (or secondary) tumors. As used herein, “primary” tumors are those located at the site where the tumor began to grow (i.e., where it originated). As used herein, “metastatic” (or “secondary”) tumors are those that have spread to other parts of body from the original tumor site. In some embodiments, the metastatic or secondary tumors are the same type of cancer as the primary tumor. In some embodiments, the metastatic or secondary tumors are not genetically identical to the primary tumor. In some embodiments of any of the methods or uses described herein, the cancer is breast cancer (e.g., breast invasive carcinoma, breast invasive ductal carcinoma), central or peripheral nervous system tissue cancer (e.g., brain cancer (e.g., astrocytoma, glioblastoma, glioma, oligoastrocytoma)), endocrine or neuroendocrine cancer (e.g., adrenal cancer (e.g., adrenocortical carcinoma, pheochromocytoma, paraganglioma), multiple neuroendocrine type I and type II tumors, parathyroid cancer, pituitary tumors, thyroid cancer (e.g., papillary thyroid cancer)), eye cancer (e.g., uveal cancer (e.g., uveal melanoma)), gastrointestinal cancer (e.g., anal cancer, bile duct cancer (e.g., cholangiocarcinoma), colorectal cancer (e.g., colon adenocarcinoma, rectal adenocarcinoma, mucinous adenocarcinoma, mucinous carcinoma), esophageal cancer (e.g., esophageal adenocarcinoma), gallbladder cancer, gastrointestinal carcinoid tumor, gastrointestinal stromal tumor, liver cancer (e.g., hepatocellular carcinoma, intrahepatic bile duct cancer), pancreatic cancer (e.g., pancreatic adenocarcinoma, pancreatic islet cell cancer), small intestine cancer, or stomach cancer (e.g., stomach adenocarcinoma, signet ring cell carcinoma of the stomach)), genitourinary cancer (e.g., bladder cancer (e.g., bladder urothelial carcinoma), kidney cancer (e.g., renal clear cell carcinoma, renal papillary cell carcinoma, kidney chromophobe), prostate cancer (e.g., prostate adenocarcinoma), testicular cancer (e.g., testicular germ cell tumors), or ureter cancer), gynecologic cancer (e.g., cervical cancer (e.g., cervical squamous cell carcinoma, endocervical adenocarcinoma, mucinous carcinoma), ovarian cancer (e.g., serous ovarian cancer, ovarian serous cystadenocarcinoma), uterine cancer (e.g., uterine carcinosarcoma, uterine endometrioid carcinoma, uterine serous carcinoma, uterine papillary serous carcinoma, uterine corpus endometrial carcinoma), or vulvar cancer), head and neck cancer (e.g., ear cancer (e.g., middle ear cancer), head and neck squamous cell carcinoma, nasal cavity cancer, oral cancer, pharynx cancer (e.g., hypopharynx cancer, nasopharynx cancer, oropharyngeal cancer), hematological cancer (e.g., leukemia (e.g., acute lymphocytic leukemia (ALL) (e.g., Philadelphia chromosome positive ALL, Philadelphia chromosome negative ALL), acute myeloid leukemia (AML) (e.g., acute promyelocytic leukemia (APL)), chronic myeloid leukemia (CML), or early T-precursor lymphoblastic leukemia, or myelodysplastic syndrome), lymphoma (e.g., Hodgkin lymphoma (e.g., nodular lymphocyte predominant Hodgkin lymphoma (NLPHL) or classic Hodgkin lymphoma), non-Hodgkin lymphoma (e.g., B cell lymphoid proliferations and lymphomas (e.g., tumor-like lesions with B-cell predominance (e.g., IgG4-related disease), precursor B cell neoplasms (e.g., B lymphoblastic lymphomas), mature B cell neoplasms (e.g., chronic lymphocytic leukemia (CLL), small lymphocytic lymphoma (SLL), marginal zone lymphoma, Burkitt lymphoma (BL), large B cell lymphoma (e.g., diffuse large B-cell lymphoma not otherwise specified (DLBCL-NOS), T-cell / histiocyte-rich large B-cell lymphoma, diffuse large B-cell lymphoma / high grade B cell lymphoma (HGBCL) (e.g., HGBCL with MYC and / or BCL2 rearrangements (HGBCL-MYC / BCL-2)), ALK-positive large B-cell lymphoma, large B cell lymphoma with IRF4 rearrangements, high-grade B cell lymphoma with 11q aberration, lymphomatoid granulomatosis, Epstein-Barr virus (EBV)- positive large B-cell lymphoma, diffuse large B-cell lymphoma associated with chronic inflammation, fibrin-associated large B-cell lymphoma, fluid-overload large B-cell lymphoma, plasmablastic lymphoma, primary large B cell lymphoma of immune-privileged sites (primary LBCL of immune-privileged sites), primary cutaneous large B-cell lymphoma leg type, intravascular large B-cell lymphoma (IVLBCL), primary mediastinal large B cell lymphoma (primary mediastinal LBCL), mediastinal grey zone lymphoma, or high grade B-cell lymphoma NOS), follicular lymphoma (FL), transformations of indolent B cell lymphomas, mantle cell lymphoma (MCL), or plasma cell neoplasms (e.g., multiple myeloma))), T-cell and NK-cell lymphoid proliferations and lymphomas (e.g., tumor-like lesions with T-cell predominance (e.g., autoimmune lymphoproliferative syndrome), precursor T-cell neoplasms (e.g., early T-precursor lymphoblastic leukemia / lymphoma or T-lymphoblastic leukemia / lymphoma NOS), mature T-cell and NK-cell neoplasms (e.g., mature T-cell and NK- cell leukemias (e.g., T-prolymphocytic leukemia, T-large granular lymphocytic leukemia, NK- large granular lymphocytic leukemia, adult T-cell leukemia / lymphoma, or aggressive NK-cell leukemia), primary cutaneous T-cell lymphoid proliferations and lymphomas (cutaneous T- cell lymphoma (CTCL)) (e.g., primary cutaneous CD4-positive small or medium T-cell lymphoproliferative disorder, primary cutaneous acral CD8-positive T-cell lymphoproliferative disorder, mycosis fungoides, Sezary syndrome, primary cutaneous CD30- positive T-cell lymphoproliferative disorder: lymphomatoid papulosis, primary cutaneous CD30-positive T-cell lymphoproliferative disorder: primary cutaneous anaplastic large cell lymphoma, subcutaneous panniculitis-like T-cell lymphoma, primary cutaneous gamma-delta T-cell lymphoma, primary cutaneous CD8-positive aggressive epidermotropic cytotoxic T-cell lymphoma, or primary cutaneous peripheral T-cell lymphoma NOS), peripheral T-cell lymphoma (PTCL) (e.g., intestinal T-cell and NK-cell lymphoid proliferations and lymphomas (e.g., indolent T-cell lymphoma of the gastrointestinal tract, indolent NK-cell lymphoproliferative disorder of the gastrointestinal tract, enteropathy-associated T-cell lymphoma, monomorphic epitheliotropic intestinal T-cell lymphoma, or intestinal T-cell lymphoma NOS)),hepatosplenic T-cell lymphoma, anaplastic large cell lymphoma (ALCL) (e.g., ALK-positive anaplastic large cell lymphoma, ALK-negative anaplastic large cell lymphoma, or breast implant-associated anaplastic large cell lymphoma), nodal T follicular helper cell lymphoma (e.g., nodal T follicular helper cell lymphoma angioimmunoblastic type (also known as angioimmunoblastic T-cell lymphoma (AITL) or follicular helper T-cell lymphoma, angioimmunoblastic type), nodal T follicular helper cell lymphoma follicular type (also known as follicular helper T-cell lymphoma, follicular type), or nodal T follicular helper cell lymphoma NOS (also known as follicular helper T-cell lymphoma, NOS)), other peripheral T-cell lymphomas (e.g., peripheral T-cell lymphoma NOS), or EBV-positive T-cell and NK- cell lymphomas (e.g., EBV-positive nodal T- and NK-cell lymphoma or extranodal NK / T-cell lymphoma)))))), Li-Fraumeni tumors, mesentery cancer (e.g., omentum cancer, peritoneal cancer), pleural cancer, respiratory cancer (e.g., larynx cancer, lung cancer (e.g., lung squamous cell carcinoma, lung adenocarcinoma, mesothelioma, non-small cell lung cancer (NSCLC)), tracheal cancer), sarcoma (e.g., bone cancer (e.g., osteosarcoma, chondrosarcoma) or soft tissue sarcoma (Ewing sarcoma, leiomyosarcoma, myxofibrosarcoma, rhabdomyosarcoma)), skin cancer (e.g., melanoma), thymus cancer (e.g., thymoma), or a combination thereof. In some embodiments, the cancer is breast cancer (e.g., breast invasive carcinoma, breast invasive ductal carcinoma), central or peripheral nervous system tissue cancer (e.g., brain cancer (e.g., astrocytoma, glioblastoma, glioma, oligoastrocytoma)), endocrine or neuroendocrine cancer (e.g., adrenal cancer (e.g., adrenocortical carcinoma, pheochromocytoma, paraganglioma), thyroid cancer (e.g., papillary thyroid cancer)), eye cancer (e.g., uveal cancer (e.g., uveal melanoma)), gastrointestinal cancer (e.g., bile duct cancer (e.g., cholangiocarcinoma), colorectal cancer (e.g., colon adenocarcinoma, rectal adenocarcinoma, mucinous adenocarcinoma, mucinous carcinoma), esophageal cancer (e.g., esophageal adenocarcinoma), liver cancer (e.g., hepatocellular carcinoma), pancreatic cancer (e.g., pancreatic adenocarcinoma), or stomach cancer (e.g., stomach adenocarcinoma, signet ring cell carcinoma of the stomach)), genitourinary cancer (e.g., bladder cancer (e.g., bladder urothelial carcinoma), kidney cancer (e.g., renal clear cell carcinoma, renal papillary cell carcinoma, kidney chromophobe), prostate cancer (e.g., prostate adenocarcinoma), or testicular cancer (e.g., testicular germ cell tumors)), gynecologic cancer (e.g., cervical cancer (e.g., cervical squamous cell carcinoma, endocervical adenocarcinoma, mucinous carcinoma), ovarian cancer (e.g., serous ovarian cancer, ovarian serous cystadenocarcinoma), or uterine cancer (e.g., uterine carcinosarcoma, uterine endometrioid carcinoma, uterine serous carcinoma, uterine papillary serous carcinoma, uterine corpus endometrial carcinoma)), head and neck cancer (e.g., head and neck squamous cell carcinoma), hematological cancer (e.g., lymphoma (e.g., Hodgkin lymphoma (e.g., nodular lymphocyte predominant Hodgkin lymphoma (NLPHL)), non-Hodgkin lymphoma (e.g., B cell lymphoid proliferations and lymphomas (e.g., mature B cell neoplasms (e.g., Burkitt lymphoma (BL), large B cell lymphoma (e.g., diffuse large B-cell lymphoma not otherwise specified (DLBCL-NOS), T- cell / histiocyte-rich large B-cell lymphoma, diffuse large B-cell lymphoma / high grade B cell lymphoma (HGBCL) (e.g., HGBCL with MYC and / or BCL2 rearrangements (HGBCL- MYC / BCL-2)), primary large B cell lymphoma of immune-privileged sites (primary LBCL of immune-privileged sites), primary mediastinal large B cell lymphoma (primary mediastinal LBCL), or high grade B-cell lymphoma NOS), follicular lymphoma (FL), or transformations of indolent B cell lymphomas)), T-cell and NK-cell lymphoid proliferations and lymphomas (e.g., mature T-cell and NK-cell neoplasms (e.g., mature T-cell and NK-cell leukemias (e.g., adult T-cell leukemia / lymphoma), primary cutaneous T-cell lymphoid proliferations and lymphomas (cutaneous T-cell lymphoma (CTCL)) (e.g., primary cutaneous CD4-positive small or medium T-cell lymphoproliferative disorder, mycosis fungoides, Sezary syndrome, primary cutaneous CD30-positive T-cell lymphoproliferative disorder: lymphomatoid papulosis, primary cutaneous CD30-positive T-cell lymphoproliferative disorder: primary cutaneous anaplastic large cell lymphoma, subcutaneous panniculitis-like T-cell lymphoma, primary cutaneous gamma-delta T-cell lymphoma, or primary cutaneous peripheral T-cell lymphoma NOS), peripheral T-cell lymphoma (PTCL) (e.g., anaplastic large cell lymphoma (ALCL) (e.g., ALK-positive anaplastic large cell lymphoma, or ALK-negative anaplastic large cell lymphoma), nodal T follicular helper cell lymphoma (e.g., nodal T follicular helper cell lymphoma angioimmunoblastic type (also known as angioimmunoblastic T-cell lymphoma (AITL) or follicular helper T-cell lymphoma, angioimmunoblastic type), nodal T follicular helper cell lymphoma follicular type (also known as follicular helper T-cell lymphoma, follicular type), or nodal T follicular helper cell lymphoma NOS (also known as follicular helper T-cell lymphoma, NOS)), or other peripheral T-cell lymphomas (e.g., peripheral T-cell lymphoma NOS)))))), respiratory cancer (e.g., lung cancer (e.g., lung squamous cell carcinoma, lung adenocarcinoma, mesothelioma, non-small cell lung cancer (NSCLC))), sarcoma (e.g., leiomyosarcoma, myxofibrosarcoma), skin cancer (e.g., melanoma), thymus cancer (e.g., thymoma), or a combination thereof. In some embodiments, the cancer is a hematological cancer (e.g., lymphoma (e.g., non- Hodgkin lymphoma (e.g., B cell lymphoid proliferations and lymphomas (e.g., mature B cell neoplasms (e.g., large B cell lymphoma (e.g., diffuse large B-cell lymphoma not otherwise specified (DLBCL-NOS), or primary mediastinal large B cell lymphoma (primary mediastinal LBCL)), follicular lymphoma (FL), or transformations of indolent B cell lymphomas)), T-cell and NK-cell lymphoid proliferations and lymphomas (e.g., mature T-cell and NK-cell neoplasms (e.g., primary cutaneous T-cell lymphoid proliferations and lymphomas (cutaneous T-cell lymphoma (CTCL)) (e.g., primary cutaneous CD4-positive small or medium T-cell lymphoproliferative disorder, mycosis fungoides, or Sezary syndrome), or peripheral T-cell lymphoma (PTCL) (e.g., nodal T follicular helper cell lymphoma (e.g., nodal T follicular helper cell lymphoma angioimmunoblastic type (also known as angioimmunoblastic T-cell lymphoma (AITL) or follicular helper T-cell lymphoma, angioimmunoblastic type), nodal T follicular helper cell lymphoma follicular type (also known as follicular helper T-cell lymphoma, follicular type), or nodal T follicular helper cell lymphoma NOS (also known as follicular helper T-cell lymphoma, NOS)), or other peripheral T-cell lymphomas (e.g., peripheral T-cell lymphoma NOS)))))), breast cancer, gastrointestinal cancer, brain cancer (e.g., glioblastoma) or lung cancer (e.g., NSCLC). In some embodiments, the cancer is a mature B cell neoplasm (e.g., chronic lymphocytic leukemia (CLL), small lymphocytic lymphoma (SLL), Burkitt lymphoma (BL), large B cell lymphoma (e.g., diffuse large B-cell lymphoma not otherwise specified (DLBCL- NOS), T-cell / histiocyte-rich large B-cell lymphoma, diffuse large B-cell lymphoma / high grade B cell lymphoma (HGBCL) (e.g., HGBCL with MYC and / or BCL2 rearrangements (HGBCL- MYC / BCL-2)), primary large B cell lymphoma of immune-privileged sites (primary LBCL of immune-privileged sites), intravascular large B-cell lymphoma (IVLBCL), primary mediastinal large B cell lymphoma (primary mediastinal LBCL), or high grade B-cell lymphoma NOS (HBGCL-NOS)), follicular lymphoma (FL), mantle cell lymphoma (MCL), or transformations of indolent B cell lymphomas), a peripheral T-cell lymphoma (PTCL) (e.g., anaplastic large cell lymphoma (ALCL) (e.g., ALK-positive anaplastic large cell lymphoma, or ALK-negative anaplastic large cell lymphoma), nodal T follicular helper cell lymphoma (e.g., nodal T follicular helper cell lymphoma angioimmunoblastic type (also known as angioimmunoblastic T-cell lymphoma (AITL) or follicular helper T-cell lymphoma, angioimmunoblastic type), nodal T follicular helper cell lymphoma follicular type (also known as follicular helper T-cell lymphoma, follicular type), or nodal T follicular helper cell lymphoma NOS (also known as follicular helper T-cell lymphoma, NOS))), a primary cutaneous T-cell lymphoid proliferation or lymphoma (cutaneous T-cell lymphoma (CTCL)) (e.g., primary cutaneous CD4-positive small or medium T-cell lymphoproliferative disorder, mycosis fungoides, Sezary syndrome, or primary cutaneous gamma-delta T-cell lymphoma), nodular lymphocyte predominant Hodgkin lymphoma (NLPHL), diffuse histiocytic lymphoma (DHL), acute lymphocytic leukemia (ALL), chronic myeloid leukemia (CML), or early T- precursor lymphoblastic leukemia. In some embodiments, the cancer is a mature B cell neoplasm (e.g., BL, large B cell lymphoma (e.g., diffuse large B-cell lymphoma not otherwise specified (DLBCL-NOS), diffuse large B-cell lymphoma / high grade B cell lymphoma (HGBCL) (e.g., HGBCL with MYC and / or BCL2 rearrangements (HGBCL-MYC / BCL-2)), primary LBCL of immune-privileged sites, primary mediastinal LBCL, or HBGCL-NOS), FL, MCL, or transformations of indolent B cell lymphomas), a peripheral T-cell lymphoma (PTCL) (e.g., anaplastic large cell lymphoma (ALCL) (e.g., ALK-positive anaplastic large cell lymphoma, or ALK-negative anaplastic large cell lymphoma), nodal T follicular helper cell lymphoma (e.g., nodal T follicular helper cell lymphoma angioimmunoblastic type (also known as angioimmunoblastic T-cell lymphoma (AITL) or follicular helper T-cell lymphoma, angioimmunoblastic type), nodal T follicular helper cell lymphoma follicular type (also known as follicular helper T-cell lymphoma, follicular type), or nodal T follicular helper cell lymphoma NOS (also known as follicular helper T-cell lymphoma, NOS))), a primary cutaneous T-cell lymphoid proliferation or lymphoma (cutaneous T-cell lymphoma (CTCL)) (e.g., primary cutaneous CD4-positive small or medium T-cell lymphoproliferative disorder, mycosis fungoides, Sezary syndrome, or primary cutaneous gamma-delta T-cell lymphoma), or ALL (e.g., B-ALL). In some embodiments, the cancer is a mature B cell neoplasm (e.g., a large B cell lymphoma (e.g., diffuse large B-cell lymphoma not otherwise specified (DLBCL- NOS), diffuse large B-cell lymphoma / high grade B cell lymphoma (HGBCL) (e.g., HGBCL with MYC and / or BCL2 rearrangements (HGBCL-MYC / BCL-2)), primary LBCL of immune- privileged sites, primary mediastinal LBCL, or HBGCL-NOS), FL, or transformations of indolent B cell lymphomas). In some embodiments, the cancer is a mature B cell neoplasm (e.g., large B cell lymphoma (e.g., diffuse large B-cell lymphoma not otherwise specified (DLBCL-NOS), diffuse large B-cell lymphoma / high grade B cell lymphoma (HGBCL) (e.g., HGBCL with MYC and / or BCL2 rearrangements (HGBCL-MYC / BCL-2)), primary LBCL of immune-privileged sites, primary mediastinal LBCL, or HBGCL-NOS), FL, MCL, or transformations of indolent B cell lymphomas), or ALL (e.g., B-ALL). In some embodiments, the cancer is a peripheral T-cell lymphoma (PTCL) (e.g., anaplastic large cell lymphoma (ALCL) (e.g., ALK-positive anaplastic large cell lymphoma, or ALK-negative anaplastic large cell lymphoma), nodal T follicular helper cell lymphoma (e.g., nodal T follicular helper cell lymphoma angioimmunoblastic type (also known as angioimmunoblastic T-cell lymphoma (AITL) or follicular helper T-cell lymphoma, angioimmunoblastic type), nodal T follicular helper cell lymphoma follicular type (also known as follicular helper T-cell lymphoma, follicular type), or nodal T follicular helper cell lymphoma NOS (also known as follicular helper T-cell lymphoma, NOS))). See, e.g., Leeman-Neill and Bhagat, Expert Opinion on Therapeutic Targets 22.2 (2018): 143-152, doi: 10.1080 / 14728222.2018.1420782; Mlynarczyk and Melnick. Immunological Reviews 288.1 (2019): 214-239, doi: 10.1111 / imr.12755; Hurtz, Christian, et al., Journal of Experimental Medicine 208.11 (2011): 2163-2174, doi: 10.1084 / jem.20110304; Deb, Dhruba, et al. Cancer Research 77.11 (2017): 3070-3081, doi: 10.1158 / 0008-5472.CAN-15-3052; Cardenas, Mariano G., et al., Clinical Cancer Research 23.4 (2017): 885-893, doi: 10.1158 / 1078-0432.CCR-16-2071; Walker, Sarah R., et al., Oncogene 34.9 (2015): 1073-1082, doi: 10.1038 / onc.2014.61; See, e.g., Alaggio, Rita, et al. Leukemia 36.7 (2022): 1720-1748, doi: 10.1038 / s41375-022-01620-2; Paik, Jin Ho, et al. Human Pathology 131 (2023): 47-60, doi: 10.1016 / j.humpath.2022.12.003; and International Publication Nos. WO 2021 / 080950, WO 2021 / 077010, and WO 2022 / 221673. In some embodiments, the cancer is a non-Hodgkin lymphoma (e.g., a mature B cell neoplasm (e.g., chronic lymphocytic leukemia (CLL), small lymphocytic lymphoma (SLL), Burkitt lymphoma (BL), large B cell lymphoma (e.g., diffuse large B-cell lymphoma not otherwise specified (DLBCL-NOS), diffuse large B-cell lymphoma / high grade B cell lymphoma (HGBCL) (e.g., HGBCL with MYC and / or BCL2 rearrangements (HGBCL- MYC / BCL-2)), primary large B cell lymphoma of immune-privileged sites (primary LBCL of immune-privileged sites), intravascular large B-cell lymphoma (IVLBCL), primary mediastinal large B cell lymphoma (primary mediastinal LBCL), or high grade B-cell lymphoma NOS (HBGCL-NOS)), follicular lymphoma (FL), mantle cell lymphoma (MCL), or transformations of indolent B cell lymphomas), a peripheral T-cell lymphoma (PTCL) (e.g., anaplastic large cell lymphoma (ALCL) (e.g., ALK-positive anaplastic large cell lymphoma, or ALK-negative anaplastic large cell lymphoma), nodal T follicular helper cell lymphoma (e.g., nodal T follicular helper cell lymphoma angioimmunoblastic type (also known as angioimmunoblastic T-cell lymphoma (AITL) or follicular helper T-cell lymphoma, angioimmunoblastic type), nodal T follicular helper cell lymphoma follicular type (also known as follicular helper T-cell lymphoma, follicular type), or nodal T follicular helper cell lymphoma NOS (also known as follicular helper T-cell lymphoma, NOS))), or a primary cutaneous T-cell lymphoid proliferation or lymphoma (cutaneous T-cell lymphoma (CTCL)) (e.g., primary cutaneous CD4-positive small or medium T-cell lymphoproliferative disorder, mycosis fungoides, Sezary syndrome, or primary cutaneous gamma-delta T-cell lymphoma)). In some embodiments, the non-Hodgkin lymphoma is B-cell non-Hodgkin lymphoma. In some embodiments, the non-Hodgkin lymphoma is CD20-positive. In some embodiments, the non- Hodgkin lymphoma is CD20-positive B-cell non-Hodgkin lymphoma. In some embodiments, the subject has not been previously treated for the non-Hodgkin lymphoma. In some embodiments, the subject has previously received chemotherapy. In some embodiments, the subject has been previously treated with rituximab or obinutuzumab as a monotherapy or in combination with an additional therapy or therapeutic agent. In some embodiments, the subject has been previously treated with rituximab as a monotherapy or in combination with an additional therapy or therapeutic agent. In some embodiments, the subject has been previously treated with obinutuzumab as a monotherapy or in combination with an additional therapy or therapeutic agent. In some embodiments, the subject has previously been treated with R-CHOP (RITUXAN® (rituximab), cyclophosphamide, hydroxydaunorubicin, vincristine, and prednisone), or G-CHOP (GAZYVA® (obinutuzumab)), cyclophosphamide, hydroxydaunorubicin, vincristine, and prednisone). In some cases, the subject has previously been treated with etoposide and R-CHOP (called R-EPOCH). In some cases, the subject has been previously treated with R-CHOP combined with lenalidomide, venetoclax, ibrutinib, acalabrutinib, obinutuzumab, polatuzumab, pembrolizumab, durvalumab, or mosunetuzumab. In some embodiments, the subject has been previously treated with cyclophosphamide, vincristine, and prednisone (CVP), with or without rituximab or obinutuzumab. In some embodiments, the subject has received one or more lines of systemic therapy. In some embodiments, the subject has received two or more lines of systemic therapy. In some embodiments, the subject has previously been treated with a cell-based therapy (e.g., adoptive cell therapy (e.g., CAR T therapy, cytokine-induced killer cells (CIKs), natural killer cells (e.g., CAR-modified NK cells)) or antibody-armed cell therapy). In some embodiments, the non- Hodgkin lymphoma is non-progressing (including stable disease) non-Hodgkin lymphoma. In some embodiments, the non-Hodgkin lymphoma is relapsed or refractory non-Hodgkin lymphoma. In some embodiments, the subject is a subject who relapsed after, or is refractory to, a rituximab-containing regimen. In some embodiments, the subject is a subject who relapsed after, or is refractory to, an obinutuzumab-containing regimen. In some such embodiments, treatment effect can be measured by progression-free survival (PFS), event-free survival (EFS), overall survival (OS), time to treatment failure, response rate (e.g., overall response rate, complete response, partial response, or a combination thereof), duration of response, or a combination thereof. In some embodiments, cancer is a non-Hodgkin lymphoma, and a compound provided herein, or a pharmaceutically acceptable salt thereof, is administered as a monotherapy. In some embodiments, the cancer is a large B cell lymphoma (e.g., diffuse large B-cell lymphoma not otherwise specified (DLBCL-NOS), diffuse large B-cell lymphoma / high grade B cell lymphoma (HGBCL) (e.g., HGBCL with MYC and / or BCL2 rearrangements (HGBCL- MYC / BCL-2)), primary LBCL of immune-privileged sites, primary mediastinal LBCL, or HBGCL-NOS). In some embodiments, the DLBCL (e.g., DLBCL-NOS) is characterized by a BCL2 translocation, a BCL6 translocation, a CD79B mutation (e.g., H225Y, A205D, Y196del, Y196F, Y196D, Y207X, Y196N, A205fs, Y196S, Y196H, A205fs, T206fs, H194_E197delinsQ, E197G, K219T, E192fs, or Y196C), an EZH2 mutation (e.g., a Y646F, Y646N, A682G, or A692V mutation), a MYC translocation, a MYD88 mutation (e.g., a L265P mutation), a NOTCH1 mutation (e.g., Q2394X, Q2501X, Q2459X, Y2490X, G2427fs, Q2444X, P2514fs, or P2517S), a NOTCH2 mutation (e.g., Q2285K, S2136fs, Q2361X, P2288fs, L2415fs, G2410fs, Q2409X, S2388X, I2304fs, Q2364X, Q2360fs, S2395X, E2261fs, M2267fs, Q2285fs, R2400X, P2303fs, Q2285fs, A2273fs, K2133fs, Q2389X, E2399X, E2290X, Q2325X, Y2340X, Y2392X, or E2411fs), a TP53 mutation (e.g., R181C, E336A, R248W, P98fs, P152L, R280I, S149fs, P151H, G245D, Y236D, S127F, A161T, D148fs, M246I, Y126C, H179R, A159P, C238G, L93fs, Y220C, R283fs, G244D, G245S, E171X, R209X, T155_R156dup, E271K, R306X, G105D, L93fs, G262V, W53X, G244V, H214Y, R282W, R337C, Q331fs, R273G, R273C, C176Y, S215R, R213Q, I195T, G245R, I232T, R175H, Y126D, R273H, R196X, Y205C, C141Y, C229X, Y126N, P278S, P151S, Y236H, R282G, Y103X, V216M, G244S, G266E, V173A, V173fs, I254S, T125M, R342X, P152fs, Y205D, V274L, L257P, C135Y, C176R, Y234N, R248Q, G244R, Y234H, R248G, M237I, R213X, E258D, V173M, L252_I254del, L252I, Y234C, or C176F), 17p deletion, 18q gain, or a combination thereof. In some embodiments, the DLBCL (e.g., DLBCL-NOS) has a BCL6 rearrangement, a NOTCH2 mutation (e.g., Q2285K, S2136fs, Q2361X, P2288fs, L2415fs, G2410fs, Q2409X, S2388X, I2304fs, Q2364X, Q2360fs, S2395X, E2261fs, M2267fs, Q2285fs, R2400X, P2303fs, Q2285fs, A2273fs, K2133fs, Q2389X, E2399X, E2290X, Q2325X, Y2340X, Y2392X, E2411fs), or a combination thereof. In some embodiments, the large B cell lymphoma (e.g., DLBCL-NOS) is large B cell lymphoma having a germinal center B cell (GCB) cell of origin. In some embodiments, the large B cell lymphoma (e.g., DLBCL- NOS) is a BN2-type large B cell lymphoma (e.g., having a BCL6 rearrangement and / or a NOTCH2 mutation). In some embodiments, the large B cell lymphoma (e.g., DLBCL-NOS) is an EZB-type large B cell lymphoma (e.g., having an EZH2 mutation and / or a BCL2 translocation). In some embodiments, the large B cell lymphoma (e.g., DLBCL-NOS) is a C1 genetic cluster large B cell lymphoma (e.g., having a BCL6 rearrangement and / or a NOTCH2 mutation). See, e.g., Schmitz, Roland, et al. New England Journal of Medicine 378.15 (2018): 1396-1407, doi: 10.1056 / NEJMoa1801445; Chapuy, Bjoern, et al. Nature Medicine 24.5 (2018): 679-690, doi: 10.1038 / s41591-018-0016-8 for additional description of these classifications. In some embodiments, the cancer is a FL. In some embodiments, the FL has a BCL2 translocation (e.g., a t(14;18) translocation). In some embodiments, the FL has an EZH2 mutation (e.g., a Y646F, Y646N, A682G, or A692V mutation). See, e.g., Kridel, Robert, Laurie H. Sehn, and Randy D. Gascoyne. The Journal of Clinical Investigation 122.10 (2012): 3424- 3431, doi: 10.1172 / JCI63186. In some embodiments, the cancer is a FL, and a compound provided herein, or a pharmaceutically acceptable salt thereof, is administered as a monotherapy. In some embodiments, the cancer is a B-ALL. In some embodiments, the B-ALL has an MLL rearrangement (e.g., an MLL-Af4 fusion, an MLL-Af6 fusion, an MLL-Af9 fusion, an MLL-ENL fusion, or an MLL-PTD fusion), is pre-B cell receptor positive (Pre-BCR+), has the Philadelphia chromosome, is Philadelphia chromosome-like, is dependent on Ras signaling, has a BCL2 amplification, has a JAK2 mutation (with or without high cytokine receptor-like factor 2 (CRLF2) expression), or a combination thereof. See, e.g., Knight, Thomas, and Julie Anne Elizabeth Irving. Frontiers in Oncology 4 (2014): 160, doi: 10.3389 / fonc.2014.00160; Geng, Huimin, et al. Cancer Cell 27.3 (2015): 409-425, doi: 10.1016 / j.ccell.2015.02.003; Jain, Nitin, et al. Blood, 129.5 (2017): 572-581, doi: 10.1182 / blood-2016-07-726588; and Hurtz, Christian, et al. Genes & Development 33 (2019): 1265-1279, doi: 10.1101 / gad.327593.119. In some embodiments, the cancer is a B-ALL, and a compound provided herein, or a pharmaceutically acceptable salt thereof, is administered as a monotherapy. In some embodiments, a compound provided herein, or a pharmaceutically acceptable salt thereof, is used in the treatment of subject having a B-ALL. In some embodiments, the B-ALL is a relapsed or refractory B-ALL after two or more lines of systemic therapy. In some embodiments, the subject has previously been treated with another anticancer agent, a chemotherapeutic agent, surgery, radiation, a multi-kinase inhibitor, or a combination thereof. In some embodiments, the cancer is a large B cell lymphoma (e.g., diffuse large B-cell lymphoma not otherwise specified (DLBCL-NOS), diffuse large B-cell lymphoma / high grade B cell lymphoma (HGBCL) (e.g., HGBCL with MYC and / or BCL2 rearrangements (HGBCL- MYC / BCL-2)), primary LBCL of immune-privileged sites, primary mediastinal LBCL, or HBGCL-NOS). In some embodiments, the subject has not been previously treated for the large B cell lymphoma (e.g., diffuse large B-cell lymphoma not otherwise specified (DLBCL-NOS), diffuse large B-cell lymphoma / high grade B cell lymphoma (HGBCL) (e.g., HGBCL with MYC and / or BCL2 rearrangements (HGBCL-MYC / BCL-2)), primary LBCL of immune- privileged sites, primary mediastinal LBCL, or HBGCL-NOS). In some embodiments, the subject has previously received chemotherapy. In some embodiments, the subject has been previously treated with rituximab or obinutuzumab as a monotherapy or in combination with an additional therapy or therapeutic agent. In some embodiments, the subject has been previously treated with rituximab as a monotherapy or in combination with an additional therapy or therapeutic agent. In some embodiments, the subject has been previously treated with obinutuzumab as a monotherapy or in combination with an additional therapy or therapeutic agent. In some embodiments, the subject has previously been treated with lenalidomide in combination with rituximab or obinutuzumab. In some embodiments, the subject has previously been treated with cyclophosphamide, vincristine and prednisone (CVP), optionally in combination with rituximab or obinutuzumab. In some embodiments, the subject has previously been treated with R-CHOP (RITUXAN® (rituximab), cyclophosphamide, hydroxydaunorubicin, vincristine, and prednisone), or G-CHOP (GAZYVA® (obinutuzumab)), cyclophosphamide, hydroxydaunorubicin, vincristine, and prednisone). In some cases, the subject has previously been treated with etoposide and R-CHOP (called R- EPOCH). In some cases, the subject has been previously treated with R-CHOP combined with lenalidomide, venetoclax, ibrutinib, acalabrutinib, obinutuzumab, polatuzumab, pembrolizumab, durvalumab, or mosunetuzumab. In some embodiments, the subject has been previously treated with a rituximab-containing regimen. In some embodiments, the subject has been previously treated with an obinutuzumab-containing regimen. In some embodiments, the subject has been previously treated with a mosunetuzumab-containing regimen. In some embodiments, the subject has been previously treated with an epcoritamab-containing regimen. In some embodiments, the subject has received one or more lines of systemic therapy. In some embodiments, the subject has received two or more lines of systemic therapy. In some embodiments, the subject has previously been treated with a cell-based therapy (e.g., adoptive cell therapy (e.g., CAR T therapy, cytokine-induced killer cells (CIKs), natural killer cells (e.g., CAR-modified NK cells)) or antibody-armed cell therapy). In some embodiments, the large B cell lymphoma (e.g., diffuse large B-cell lymphoma not otherwise specified (DLBCL-NOS), diffuse large B-cell lymphoma / high grade B cell lymphoma (HGBCL) (e.g., HGBCL with MYC and / or BCL2 rearrangements (HGBCL-MYC / BCL-2)), primary LBCL of immune- privileged sites, primary mediastinal LBCL, or HBGCL-NOS) is non-progressing (including stable disease) LBCL. In some embodiments, the large B cell lymphoma (e.g., diffuse large B- cell lymphoma not otherwise specified (DLBCL-NOS), diffuse large B-cell lymphoma / high grade B cell lymphoma (HGBCL) (e.g., HGBCL with MYC and / or BCL2 rearrangements (HGBCL-MYC / BCL-2)), primary LBCL of immune-privileged sites, primary mediastinal LBCL, or HBGCL-NOS), is relapsed or refractory LBCL. In some embodiments, the subject is a subject who relapsed after, or is refractory to, a rituximab-containing regimen. In some embodiments, the subject is a subject who relapsed after, or is refractory to, an obinutuzumab- containing regimen. In some such embodiments, treatment effect can be measured by progression-free survival (PFS), event-free survival (EFS), overall survival (OS), time to treatment failure, response rate (e.g., overall response rate, complete response, partial response, or a combination thereof), duration of response, or a combination thereof. In some embodiments, the cancer is a large B cell lymphoma (e.g., diffuse large B-cell lymphoma not otherwise specified (DLBCL-NOS), diffuse large B-cell lymphoma / high grade B cell lymphoma (HGBCL) (e.g., HGBCL with MYC and / or BCL2 rearrangements (HGBCL- MYC / BCL-2)), primary LBCL of immune-privileged sites, primary mediastinal LBCL, or HBGCL-NOS), and a compound provided herein, or a pharmaceutically acceptable salt thereof, is administered as a monotherapy. In some embodiments, a compound provided herein, or a pharmaceutically acceptable salt thereof is used in the treatment of subject having a large B cell lymphoma (e.g., diffuse large B-cell lymphoma not otherwise specified (DLBCL-NOS), diffuse large B-cell lymphoma / high grade B cell lymphoma (HGBCL) (e.g., HGBCL with MYC and / or BCL2 rearrangements (HGBCL-MYC / BCL-2)), primary LBCL of immune- privileged sites, primary mediastinal LBCL, or HBGCL-NOS). In some embodiments, the large B cell lymphoma (e.g., diffuse large B-cell lymphoma not otherwise specified (DLBCL- NOS), diffuse large B-cell lymphoma / high grade B cell lymphoma (HGBCL) (e.g., HGBCL with MYC and / or BCL2 rearrangements (HGBCL-MYC / BCL-2)), primary LBCL of immune- privileged sites, primary mediastinal LBCL, or HBGCL-NOS) is a relapsed or refractory LBCL after two or more lines of systemic therapy. In some embodiments, the cancer is a FL. In some embodiments, the subject has not been previously treated for the FL. In some embodiments, the subject has previously received chemotherapy. In some embodiments, the subject has been previously treated with rituximab or obinutuzumab as a monotherapy or in combination with an additional therapy or therapeutic agent. In some embodiments, the subject has been previously treated with rituximab as a monotherapy or in combination with an additional therapy or therapeutic agent. In some embodiments, the subject has been previously treated with obinutuzumab as a monotherapy or in combination with an additional therapy or therapeutic agent. In some embodiments, the subject has previously been treated with rituximab or obinutuzumab monotherapy. In some embodiments, the subject has previously been treated with bendamustine in combination with rituximab or obinutuzumab. In some embodiments, the subject has previously been treated with lenalidomide in combination with rituximab or obinutuzumab (the combination of lenalidomide with rituximab is sometimes called “R2”). In some embodiments, the subject has previously been treated with cyclophosphamide, vincristine and prednisone (CVP), optionally in combination with rituximab or obinutuzumab. In some embodiments, the subject has previously been treated with R-CHOP or G-CHOP. In some embodiments, the subject has received one or more lines of systemic therapy. In some embodiments, the subject has received two or more lines of systemic therapy. In some embodiments, the subject has previously been treated with a cell-based therapy (e.g., adoptive cell therapy (e.g., CAR T therapy, cytokine- induced killer cells (CIKs), natural killer cells (e.g., CAR-modified NK cells)) or antibody- armed cell therapy). In some embodiments, the non-Hodgkin lymphoma is non-progressing (including stable disease) FL. In some embodiments, the FL is relapsed or refractory FL. In some embodiments, the subject is a subject who relapsed after, or is refractory to, a rituximab- containing regimen. In some embodiments, the subject is a subject who relapsed after, or is refractory to, an obinutuzumab-containing regimen. In some such embodiments, treatment effect can be measured by progression-free survival (PFS), event-free survival (EFS), overall survival (OS), time to treatment failure, response rate (e.g., overall response rate, complete response, partial response, or a combination thereof), duration of response, or a combination thereof. In some embodiments, the cancer is a FL, and a compound provided herein, or a pharmaceutically acceptable salt thereof, is administered as a monotherapy. In some embodiments, a compound provided herein, or a pharmaceutically acceptable salt thereof is used in the treatment of subject having a FL. In some embodiments, the FL is a relapsed or refractory FL after two or more lines of systemic therapy. In some embodiments, the cancer is a BL. In some embodiments, the subject has not been previously treated for the BL. In some embodiments, the subject has previously received chemotherapy. In some embodiments, the subject has been previously treated with rituximab or obinutuzumab as a monotherapy or in combination with an additional therapy or therapeutic agent. In some embodiments, the subject has been previously treated with rituximab as a monotherapy or in combination with an additional therapy or therapeutic agent. In some embodiments, the subject has been previously treated with obinutuzumab as a monotherapy or in combination with an additional therapy or therapeutic agent. In some embodiments, the subject has previously been treated with rituximab or obinutuzumab monotherapy. In some embodiments, the subject has previously been treated with bendamustine in combination with rituximab or obinutuzumab. In some embodiments, the subject has previously been treated with R-CHOP or G-CHOP. In some embodiments, the subject has previously been treated with rituximab, cyclophosphamide, vincristine, doxorubicin, and methotrexate (R-CODOX-M). In some embodiments, the subject has previously been treated with rituximab, ifosfamide, etoposide, and cytarabine (R-IVAC). In some embodiments, the subject has previously been treated with rituximab with dose-adjusted etoposide, prednisolone, vincristine, cyclophosphamide, and doxorubicin (DA-EPOCH-R). In some embodiments, the subject has received one or more lines of systemic therapy. In some embodiments, the subject has received two or more lines of systemic therapy. In some embodiments, the subject has previously been treated with a cell-based therapy (e.g., adoptive cell therapy (e.g., CAR T therapy, cytokine- induced killer cells (CIKs), natural killer cells (e.g., CAR-modified NK cells)) or antibody- armed cell therapy). In some embodiments, the BL is non-progressing (including stable disease) BL. In some embodiments, the BL is relapsed or refractory BL. In some embodiments, the subject is a subject who relapsed after, or is refractory to, a rituximab-containing regimen. In some embodiments, the subject is a subject who relapsed after, or is refractory to, an obinutuzumab-containing regimen. In some such embodiments, treatment effect can be measured by progression-free survival (PFS), event-free survival (EFS), overall survival (OS), time to treatment failure, response rate (e.g., overall response rate, complete response, partial response, or a combination thereof), duration of response, or a combination thereof. In some embodiments, the cancer is a BL, and a compound provided herein, or a pharmaceutically acceptable salt thereof, is administered as a monotherapy. In some embodiments, a compound provided herein, or a pharmaceutically acceptable salt thereof is used in the treatment of subject having a BL. In some embodiments, the BL is a relapsed or refractory BL after two or more lines of systemic therapy. In some embodiments, the cancer is a peripheral T-cell lymphoma (PTCL) (e.g., anaplastic large cell lymphoma (ALCL) (e.g., ALK-positive anaplastic large cell lymphoma, or ALK-negative anaplastic large cell lymphoma), nodal T follicular helper cell lymphoma (e.g., nodal T follicular helper cell lymphoma angioimmunoblastic type (also known as angioimmunoblastic T-cell lymphoma (AITL) or follicular helper T-cell lymphoma, angioimmunoblastic type), nodal T follicular helper cell lymphoma follicular type (also known as follicular helper T-cell lymphoma, follicular type), or nodal T follicular helper cell lymphoma NOS (also known as follicular helper T-cell lymphoma, NOS))) or a primary cutaneous T-cell lymphoid proliferation or lymphoma (cutaneous T-cell lymphoma (CTCL)) (e.g., primary cutaneous CD4-positive small or medium T-cell lymphoproliferative disorder, mycosis fungoides, Sezary syndrome, or primary cutaneous gamma-delta T-cell lymphoma) In some embodiments, the subject has not been previously treated for the PTCL or CTCL. In some embodiments, the subject has previously received chemotherapy. In some embodiments, the subject has been previously treated with rituximab or obinutuzumab as a monotherapy or in combination with an additional therapy or therapeutic agent. In some embodiments, the subject has been previously treated with rituximab as a monotherapy or in combination with an additional therapy or therapeutic agent. In some embodiments, the subject has been previously treated with obinutuzumab as a monotherapy or in combination with an additional therapy or therapeutic agent. In some embodiments, the subject has previously been treated with rituximab or obinutuzumab monotherapy. In some embodiments, the subject has previously been treated with bendamustine in combination with rituximab or obinutuzumab. In some embodiments, the subject has previously been treated with lenalidomide in combination with rituximab or obinutuzumab (the combination with rituximab is sometimes called “R2”). In some embodiments, the subject has previously been treated with cyclophosphamide, vincristine and prednisone (CVP), optionally in combination with rituximab or obinutuzumab (R-CVP or G- CVP, respectively). In some embodiments, the subject has previously been treated with R- CHOP or G-CHOP. In some embodiments, the subject has received one or more lines of systemic therapy. In some embodiments, the subject has received two or more lines of systemic therapy. In some embodiments, the subject has previously been treated with a cell-based therapy (e.g., adoptive cell therapy (e.g., CAR T therapy, cytokine-induced killer cells (CIKs), natural killer cells (e.g., CAR-modified NK cells)) or antibody-armed cell therapy). In some embodiments, the PTCL or CTCL is non-progressing (including stable disease) PTCL or CTCL. In some embodiments, the PTCL or CTCL is relapsed or refractory PTCL or CTCL. In some embodiments, the subject is a subject who relapsed after, or is refractory to, a rituximab- containing regimen. In some embodiments, the subject is a subject who relapsed after, or is refractory to, an obinutuzumab-containing regimen. In some such embodiments, treatment effect can be measured by progression-free survival (PFS), event-free survival (EFS), overall survival (OS), time to treatment failure, response rate (e.g., overall response rate, complete response, partial response, or a combination thereof), duration of response, or a combination thereof. In some embodiments, the cancer is a PTCL or CTCL, and a compound provided herein, or a pharmaceutically acceptable salt thereof, is administered as a monotherapy. In some embodiments, a compound provided herein, or a pharmaceutically acceptable salt thereof is used in the treatment of a subject having a PTCL or CTCL. In some embodiments, the PTCL or CTCL is a relapsed or refractory PTCL or CTCL after two or more lines of systemic therapy. In some embodiments, the cancer is B-ALL. In some embodiments, the B-ALL is Philadelphia chromosome positive B-ALL. In some embodiments, the B-ALL is Philadelphia chromosome negative B-ALL. In some embodiments, the subject has previously received chemotherapy. In some embodiments, the subject has previously been treated with at least one cycle of induction, consolidation, intensification, and optional maintenance. In some cases, induction therapy can include an anthracycline, vincristine, a corticosteroid, and cyclophosphamide. In some embodiments, the anthracycline is doxorubicin. In some embodiments, the corticosteroid is dexamethasone. In some cases, the combination of doxorubicin, vincristine, dexamethasone, and cyclophosphamide is known as CVAD. In some embodiments, induction therapy can further include a tyrosine kinase inhibitor (e.g., a BCR- ABL inhibitor for subjects with this fusion). In some embodiments, induction therapy can further include asparaginase (e.g., for pediatric subjects). In some cases, consolidation therapy can include methotrexate, cytarabine, vincristine, 6-mercaptopurine, 6-thioguanine, cyclophosphamide, and etoposide. In some embodiments, consolidation therapy can further include a tyrosine kinase inhibitor (e.g., a BCR-ABL inhibitor for subjects with this fusion). In some embodiments, consolidation therapy can further include asparaginase (e.g., for pediatric subjects). In some cases, intensification therapy can include an anthracycline, vincristine, a corticosteroid, and cyclophosphamide. In some embodiments, intensification therapy can further include a tyrosine kinase inhibitor (e.g., a BCR-ABL inhibitor for subjects with this fusion). In some embodiments, intensification therapy can further include asparaginase (e.g., for pediatric subjects). Typically, pediatric and young adult regimens include higher cumulative doses of asparaginase and vincristine but can have lower cumulative doses of anthracycline and cyclophosphamide compared to adult regimens. In any of these cycle phases, an anti-CD20 immunotherapy (e.g., rituximab) can be added for subjects expressing the CD20 protein on the cells. See, e.g., Muffly, Lori, and Emily Curran. Hematology 2014, the American Society of Hematology Education Program Book 2019.1 (2019): 17-23, doi: 10.1182 / hematology.2019000009. In some embodiments, the subject has received one or more lines of systemic therapy. In some embodiments, the subject has received two or more lines of systemic therapy. In some embodiments, the B-ALL is relapsed or refractory B-ALL. In some such embodiments, treatment effect can be measured by progression-free survival (PFS), event- free survival (EFS), overall survival (OS), time to treatment failure, response rate (e.g., overall response rate, complete response, partial response, or a combination thereof), duration of response, or a combination thereof. In some embodiments, the cancer is a B-ALL, and a compound provided herein, or a pharmaceutically acceptable salt thereof, is administered as a monotherapy. In some embodiments, a compound provided herein, or a pharmaceutically acceptable salt thereof is used in the treatment of subject having a B-ALL. In some embodiments, the B-ALL is a relapsed or refractory B-ALL after two or more lines of systemic therapy. Also provided herein is a method of treating a subject having a cancer, wherein the method comprises: administering a therapeutically effective amount of a compound provided herein, or a pharmaceutically acceptable salt thereof, as a monotherapy or in conjunction with a first anticancer agent to the subject who has been administered one or more doses of the first anticancer agent for a period of time. Also provided herein is a method of treating a subject having a cancer, wherein the method comprises: (a) administering one or more doses of a first anticancer agent to the subject for a period of time; and (b) after (a), administering a therapeutically effective amount of a compound provided herein, or a pharmaceutically acceptable salt thereof, as a monotherapy or in conjunction with the first anticancer agent to the subject. Also provided herein is a method of treating a subject having a cancer, wherein the method comprises: (a) administering one or more doses of a first anticancer agent to the subject for a period of time; and (b) after (a), administering a therapeutically effective amount of a compound provided herein, or a pharmaceutically acceptable salt thereof, as a monotherapy or in conjunction with a second anticancer agent to the subject. In some embodiments of any of the methods of treating cancers provided herein, the compound provided herein, or a pharmaceutically acceptable salt thereof, is dosed q.d. (once daily) to the subject. In some embodiments of any of the methods of treating cancers provided herein, the compound provided herein, or a pharmaceutically acceptable salt thereof, is dosed b.i.d. (twice daily) to the subject. In some embodiments of any of the methods of treating cancers provided herein, the compound provided herein, or a pharmaceutically acceptable salt thereof, is dosed t.i.d. (three times daily) to the subject. In some embodiments of any of the methods of treating cancers provided herein, the compound provided herein, or a pharmaceutically acceptable salt thereof, is dosed q.i.d. (four times daily) to the subject. In some embodiments of any of the methods of treating cancers provided herein, the compound provided herein, or a pharmaceutically acceptable salt thereof, is dosed q.o.d. (every other day) to the subject. In some embodiments of any of the methods of treating cancers provided herein, the compound provided herein, or a pharmaceutically acceptable salt thereof, is dosed q.week (once weekly) to the subject. In some embodiments of any of the methods of treating cancers provided herein, the compound provided herein, or a pharmaceutically acceptable salt thereof, is dosed b.i.w. (twice weekly) to the subject. In some embodiments of any of the methods of treating cancers provided herein, the compound provided herein, or a pharmaceutically acceptable salt thereof, is dosed t.i.w. (three times weekly) to the subject. BCL6 activity has also been implicated in autoimmunity. See, for example, Li, Qing, et al. European Journal of Immunology 50.4 (2020): 525-536, doi: 10.1002 / eji.201948299; Pearce, Andrew C., et al. Journal of Biological Chemistry 297.2 (2021): 100928, doi: 10.1016 / j.jbc.2021.100928; Venkatadri, Rajkumar, et al. European Journal of Immunology 52.5 (2022): 825-834, doi: 10.1002 / eji.202149324; Patel, Preeyam S., et al. Science Advances 8.25 (2022): eabo1782, doi: 10.1126 / sciadv.abo1782; Ding, Shu, Yu Rao, and Qianjin Lu. Cellular & Molecular Immunology 19 (2022): 863-865, doi: 10.1038 / s41423-022-00882-1. Accordingly, also provided herein is a method of treating or preventing an autoimmune disease or condition in a subject in need thereof, the method comprising administering to the subject a therapeutically effective amount of a compound provided herein, or a pharmaceutically acceptable salt thereof, or a pharmaceutical composition comprising a compound provided herein, or a pharmaceutically acceptable salt thereof. Provided herein is use of a compound provided herein, or a pharmaceutically acceptable salt thereof, or a pharmaceutical composition thereof, for the treatment or prevention of an autoimmune disease or condition, for example, any of the autoimmune diseases or conditions provided herein. Provided herein is use of a compound provided herein, or a pharmaceutically acceptable salt thereof, or a pharmaceutical composition thereof, as a medicament for the treatment or prevention of an autoimmune disease or condition, for example, any of the autoimmune diseases or conditions provided herein. Provided herein is use of a compound provided herein, or a pharmaceutically acceptable salt thereof, in the manufacture of a medicament for the treatment or prevention of an autoimmune diseases or condition, for example, any of the autoimmune diseases or conditions provided herein. Provided herein is a compound provided herein, or a pharmaceutically acceptable salt thereof, or a pharmaceutical composition thereof, for use as a medicament for the treatment or prevention of an autoimmune disease or condition, for example, any of the autoimmune diseases or conditions provided herein. Provided herein is a compound provided herein, or a pharmaceutically acceptable salt thereof, or a pharmaceutical composition thereof, for use in treating or preventing an autoimmune disease or condition, for example, any of the autoimmune diseases or conditions provided herein. In some embodiments, the autoimmune disease or condition is acquired hemophilia, Addison's disease, ankylosing spondylitis, anti-neutrophil cytoplasmic antibody associated vasculitis (ANCA vasculitis), anti-synthetase syndrome, atherosclerosis, autoimmune hemolytic anemia, autoimmune hepatitis, autoimmune sclerosing cholangitis, autoimmune thyroiditis, autoimmune uveitis, Crohn’s disease, dermatomyositis, diffuse scleroderma, Goodpasture’s syndrome, graft-versus-host disease (GVHD) (e.g., chronic graft-versus-host disease (cGVHD)), Graves’ disease, Guillain-Barre syndrome, Hashimoto’s thyroiditis, Hughes’ syndrome, IgG4-related disease, immune thrombocytopenic purpura (ITP), inflammatory bowel disease, limited scleroderma, multiple sclerosis, myasthenia gravis (MG), neuromyelitis optica spectrum disorders (NMOSD) (e.g., neuromyelitis optica (NMO)), pemphigoid, pemphigus, pernicious anemia, polymyositis, primary biliary cirrhosis, psoriasis, psoriatic arthritis, rheumatoid arthritis, seronegative spondyloarthropathies, Sjogren’s syndrome, systemic lupus erythematosus, thrombocytopenic purpura, Type 1 diabetes, ulcerative colitis, vitiligo, or a combination thereof. In some embodiments, the autoimmune disease or condition is rheumatoid arthritis, systemic lupus erythematosus, or a combination thereof. In some embodiments, the autoimmune disease or condition is ANCA vasculitis, GVHD (e.g., cGVHD), myasthenia gravis, NMO, or a combination thereof. In some embodiments, the autoimmune disease or condition is ANCA vasculitis, anti-synthetase syndrome, arthritis (e.g., rheumatoid arthritis or inflammatory arthritis), GVHD (e.g., cGVHD), IgG4-RD, lupus (e.g., lupus erythematosus), ITP, MG (e.g., muscle-specific tyrosine kinase (MuSK) positive MG), MS, NMOSD (e.g., NMO), pemphigus (e.g., pemphigus vulgaris), Sjogren’s syndrome, or a combination thereof. In some embodiments, the autoimmune disease or condition is ANCA vasculitis, anti-synthetase syndrome, GVHD (e.g., cGVHD), TIP, MG (e.g., muscle-specific tyrosine kinase (MuSK) positive MG), NMOSD (e.g., NMO), pemphigus, or a combination thereof. In some embodiments, the autoimmune disease or condition is arthritis (e.g., rheumatoid arthritis or inflammatory arthritis), GVHD (e.g., cGVHD), IgG4-RD, lupus (e.g., lupus erythematosus), MG (e.g., muscle-specific tyrosine kinase (MuSK) positive MG), MS, NMOSD (e.g., NMO), pemphigus (e.g., pemphigus vulgaris), Sjogren’s syndrome, or a combination thereof See, e.g., Pearce, Andrew C., et al. Journal of Biological Chemistry 297.2 (2021): 100928, doi: 10.1016 / j.jbc.2021.100928; Ding, Shu, Yu Rao, and Qianjin Lu, Cellular & Molecular Immunology (2022): 863–865; doi: 10.1038 / s41423-022-00882-1; Lee, Dennis SW, Olga L. Rojas, and Jennifer L. Gommerman, Nature Reviews Drug Discovery 20.3 (2021): 179-199, doi: 10.1038 / s41573-020-00092-2; and International Publication Nos. WO 2020 / 014599; WO 2021 / 074620. In some embodiments of any of the methods of treating or preventing autoimmune diseases or conditions provided herein, the compound provided herein, or a pharmaceutically acceptable salt thereof, is dosed q.d. (once daily) to the subject. In some embodiments of any of the methods of treating or preventing autoimmune diseases or conditions provided herein, the compound provided herein, or a pharmaceutically acceptable salt thereof, is dosed b.i.d. (twice daily) to the subject. In some embodiments of any of the methods of treating or preventing autoimmune diseases or conditions provided herein, the compound provided herein, or a pharmaceutically acceptable salt thereof, is dosed t.i.d. (three times daily) to the subject. In some embodiments of any of the methods of treating or preventing autoimmune diseases or conditions provided herein, the compound provided herein, or a pharmaceutically acceptable salt thereof, is dosed q.i.d. (four times daily) to the subject. In some embodiments of any of the methods of treating or preventing autoimmune diseases or conditions provided herein, the compound provided herein, or a pharmaceutically acceptable salt thereof, is dosed q.o.d. (every other day) to the subject. In some embodiments of any of the methods of treating or preventing autoimmune diseases or conditions provided herein, the compound provided herein, or a pharmaceutically acceptable salt thereof, is dosed q.week (once weekly) to the subject. In some embodiments of any of the methods of treating or preventing autoimmune diseases or conditions provided herein, the compound provided herein, or a pharmaceutically acceptable salt thereof, is dosed b.i.w. (twice weekly) to the subject. In some embodiments of any of the methods of treating or preventing autoimmune diseases or conditions provided herein, the compound provided herein, or a pharmaceutically acceptable salt thereof, is dosed t.i.w. (three times weekly) to the subject. Also provided herein is a method of treating a lymphoproliferative disorder in a subject in need thereof, the method comprising administering to the subject a therapeutically effective amount of a compound provided herein, or a pharmaceutically acceptable salt thereof, or a pharmaceutical composition comprising a compound provided herein, or a pharmaceutically acceptable salt thereof. Provided herein is use of a compound provided herein, or a pharmaceutically acceptable salt thereof, or a pharmaceutical composition thereof, for the treatment of a lymphoproliferative disorder, for example, any of the lymphoproliferative disorders provided herein. Provided herein is use of a compound provided herein, or a pharmaceutically acceptable salt thereof, or a pharmaceutical composition thereof, as a medicament for the treatment of a lymphoproliferative disorder, for example, any of the lymphoproliferative disorders provided herein. Provided herein is use of a compound provided herein, or a pharmaceutically acceptable salt thereof, in the manufacture of a medicament for the treatment of a lymphoproliferative disorder, for example, any of the lymphoproliferative disorders provided herein. Provided herein is a compound provided herein, or a pharmaceutically acceptable salt thereof, or a pharmaceutical composition thereof, for use as a medicament for the treatment of a lymphoproliferative disorder, for example, any of the lymphoproliferative disorders provided herein. Provided herein is a compound provided herein, or a pharmaceutically acceptable salt thereof, or a pharmaceutical composition thereof, for use in treating a lymphoproliferative disorder, for example, any of the lymphoproliferative disorders provided herein. In some embodiments, the lymphoproliferative disorder is Epstein-Barr Virus- associated lymphoproliferative disorder. Also provided is a method for modulating (e.g., decreasing) BCL6 protein activity in a cell, comprising contacting the cell with a compound provided herein, or a pharmaceutically acceptable salt thereof. In some embodiments, the contacting is in vitro. In some embodiments, the contacting is in vivo. In some embodiments, the contacting is ex vivo. In some embodiments, the contacting is in vivo, wherein the method comprises administering an effective amount of a compound provided herein, or a pharmaceutically acceptable salt thereof, to a subject. In some embodiments, the cell is a cancer cell. In some embodiments, the cell is a mammalian cell. In some embodiments, the cell is a mammalian cancer cell. In some embodiments, the cancer cell is any cancer as described herein. As used herein, the term “contacting” refers to the bringing together of indicated moieties in an in vitro system, an in vivo system, or an ex vivo system. For example, “contacting” a cell with a compound provided herein includes the administration of a compound provided herein to the cell, in vitro or in vivo, including, for example, introducing a compound provided herein into a sample containing cells (e.g., grown in culture or derived from a subject), an organoid, or an organism (e.g., an animal (e.g., an animal bearing a tumor), or a human). Also provided is a method of modulating (e.g., decreasing) the level of BCL6 protein in a cell, comprising contacting the cell with a compound provided herein, or a pharmaceutically acceptable salt thereof. In some embodiments, the level of BCL6 protein is decreased by at least 30% (e.g., at least 40%, at least 50%, at least 60%, at least 70%, at least 80%, at least 90%, at least 95%, at least 97%, or at least 99%) compared to a cell not contacted with the compound provided herein, or a pharmaceutically acceptable salt thereof. In some embodiments, the contacting is in vitro. In some embodiments, the contacting is in vivo. In some embodiments, the contacting is in vivo, wherein the method comprises administering an effective amount of a compound provided herein, or a pharmaceutically acceptable salt thereof, to a subject having a cell having a BCL6 protein. In some embodiments, the cell is a cancer cell. In some embodiments, the cell is a mammalian cell. In some embodiments, the cell is a mammalian cancer cell. In some embodiments, the cancer cell is any cancer as described herein. Also provided is a method of inducing ubiquitination of a BCL6 protein in a cell, comprising contacting the cell with a compound provided herein, or a pharmaceutically acceptable salt thereof. In some embodiments, the contacting is in vitro. In some embodiments, the contacting is in vivo. In some embodiments, the contacting is in vivo, wherein the method comprises administering an effective amount of a compound provided herein, or a pharmaceutically acceptable salt thereof, to a subject having a cell having a BCL6 protein. In some embodiments, the cell is a cancer cell. In some embodiments, the cell is a mammalian cell. In some embodiments, the cell is a mammalian cancer cell. In some embodiments, the cancer cell is any cancer as described herein. Also provided is a method of forming a ternary complex comprising a BCL6 protein, a compound provided herein, or a pharmaceutically acceptable salt thereof, and a CRBN protein or fragment thereof in a cell, comprising contacting the cell with a compound provided herein, or a pharmaceutically acceptable salt thereof. In some embodiments, the contacting is in vitro. In some embodiments, the contacting is in vivo. In some embodiments, the contacting is in vivo, wherein the method comprises administering an effective amount of a compound provided herein, or a pharmaceutically acceptable salt thereof, to a subject having a cell having a BCL6 protein. In some embodiments, the cell is a cancer cell. In some embodiments, the cell is a mammalian cell. In some embodiments, the cell is a mammalian cancer cell. In some embodiments, the cancer cell is any cancer as described herein. Also provided herein is a method for inducing degradation of a BCL6 protein in a mammalian cell, the method comprising contacting the mammalian cell with an effective amount of a compound provided herein, or a pharmaceutically acceptable salt thereof. Also provided herein is a method of inhibiting cell proliferation, in vitro or in vivo, the method comprising contacting a cell with an effective amount of a compound provided herein, or a pharmaceutically acceptable salt thereof, or a pharmaceutical composition thereof as defined herein. Further provided herein is a method of increasing cell death, in vitro or in vivo, the method comprising contacting a cell with an effective amount of a compound provided herein, or a pharmaceutically acceptable salt thereof, or a pharmaceutical composition thereof as defined herein. Also provided herein is a method of increasing tumor cell death in a subject, the method comprising administering to the subject a compound provided herein, or a pharmaceutically acceptable salt thereof, in an amount effective to increase tumor cell death. When employed as pharmaceuticals, the compounds provided herein, or pharmaceutically acceptable salts thereof, can be administered in the form of pharmaceutical compositions as described herein. Combinations In any of the indications described herein, a compound provided herein, or a pharmaceutically acceptable salt thereof, can be used as a monotherapy. In some embodiments, a compound provided herein, or a pharmaceutically acceptable salt thereof, can be used prior to administration of an additional therapeutic agent or additional therapy. For example, a subject in need thereof can be administered one or more doses of a compound provided herein, or a pharmaceutically acceptable salt thereof, for a period of time and then undergo at least partial resection of the tumor. In some embodiments, the treatment with one or more doses of a compound provided herein, or a pharmaceutically acceptable salt thereof, reduces the size of the tumor (e.g., the tumor burden) prior to the at least partial resection of the tumor. In some embodiments, a subject in need thereof can be administered one or more doses of a compound provided herein, or a pharmaceutically acceptable salt thereof, for a period of time and undergo one or more rounds of radiation therapy. In some embodiments, the treatment with one or more doses of a compound provided herein, or a pharmaceutically acceptable salt thereof, reduces the size of the tumor (e.g., the tumor burden) prior to the one or more rounds of radiation therapy. In some embodiments of any the methods described herein, the compound provided herein, or a pharmaceutically acceptable salt thereof, is administered in combination with a therapeutically effective amount of at least one additional therapeutic (e.g., chemotherapeutic) agent. Non-limiting examples of additional therapeutic agents include: RAS pathway targeted therapeutic agents (e.g., Ras / RAF / MEK / PI3K pathway inhibitors, (e.g., Ras inhibitors, KRas- targeted therapeutic agents, SOS1 inhibitors, SOS1 / Ras protein-protein interaction inhibitors, SHP2 inhibitors, PI3K-AKT-mTOR pathway inhibitors)), kinase-targeted therapeutics (e.g., MEK inhibitors, ERK inhibitors, Raf inhibitors (e.g., BRaf inhibitors), PI3K inhibitors, AKT inhibitors, BTK inhibitors, mTOR inhibitors, CDK4 / 5 inhibitors, CDK4 / 6 inhibitors, MET inhibitors, JAK inhibitors (e.g., JAK2 inhibitors), FAK inhibitors, ErbB family inhibitors (e.g., EGFR inhibitors, Her2 inhibitors), Src inhibitors), menin inhibitors, mTORC1 inhibitors, YAP inhibitors, proteasome inhibitors, farnesyl transferase inhibitors, HSP90 inhibitors, PTEN inhibitors, inhibitors of the polycomb repressive complex 2 (PRC2) (e.g., EZH1 / 2 or EZH2 inhibitors), signal transduction pathway inhibitors, checkpoint inhibitors, modulators of the apoptosis pathway (e.g., BCL-2 inhibitors, BCL-XL inhibitors), XPO1 inhibitors, steroids, chemotherapeutics, angiogenesis-targeted therapies, immune-targeted agents including immunomodulatory imide drugs (sometimes called “IMiDs” or “CELMoDs”), immunotherapy (e.g., anti-PD1, anti-PD-L1, anti-CD19, anti-CD20, anti-CD22, anti-CD3, anti-CD30, anti- CD79B, or anti-CD47 therapies, including antibodies (e.g., single-targeted antibodies targeting one or more of PD1, PD-L1, CD19, CD20, CD22, CD3, CD30, CD79B, or CD47, bispecific antibodies (including bispecific T cell engagers (BiTEs)) targeting one or more of PD1, PD- L1, CD19, CD20, CD22, CD3, CD30, CD79B, or CD47, and antibody-drug conjugates (ADCs) incorporating one or more of PD1, PD-L1, CD19, CD20, CD22, CD3, CD30, CD79B, or CD47 antibodies ) or antigen-binding fragments thereof, a PD-1 inhibitor, or a PD-L1 inhibitor), cell-based therapeutics (e.g., adoptive cell therapy (e.g., CAR T therapy, cytokine- induced killer cells (CIKs), natural killer cells (e.g., CAR-modified NK cells)) or antibody- armed cell therapy), and radiotherapy. As used herein, a biosimilar antibody refers to an antibody or antigen-binding fragment that has the same primary amino acid sequence as compared to a reference antibody and optionally, can have detectable differences in post-translation modifications (e.g., glycosylation and / or phosphorylation) as compared to the reference antibody (e.g., a different glycoform). In some embodiments, the additional therapeutic agent is a PI3K inhibitor, an Abl inhibitor (e.g., a BCR-Abl inhibitor), a BTK inhibitor, a JAK inhibitor (e.g., a JAK2 inhibitor), a BRaf inhibitor, a MEK inhibitor, a menin inhibitor, a BCL-2 inhibitor, a BCL-XL inhibitor, an MCL-1 inhibitor, an XPO1 inhibitor, an inhibitor of the polycomb repressive complex 2 (e.g., an EZH1 / 2 or EZH2 inhibitor), an immunomodulatory imide drug, a steroid, anti-CD19 therapy, anti-CD20 therapy, anti-CD3 therapy, chemotherapy, or a combination thereof. Without being bound by any particular theory, it is believed that targeting BCL6 can result in the induction of genes that it typically represses, such as BCL2. In some embodiments, the additional therapeutic agent is a BCL-2 inhibitor (e.g., foselutoclax (UBX-1325), lacutoclax, lisaftoclax, navitoclax, obatoclax, pelcitoclax, venetoclax, sonrotoclax (BGB- 11417), surzetoclax, oblimersen (e.g., oblimersen sodium), beclanorsen, AZD-0466, ICP-248, TQB-3909, UBX-1967, ZN-d5, or a combination thereof). In some embodiments, the PI3K inhibitor is alpelisib (BYL719), amdizalisib, apitolisib (GDC-0980), bimiralisib, buparlisib (BKM120), copanlisib (ALIQOPA™, BAY80-6946) (e.g., copanlisib dihydrochloride or a hydrate of copanlisib dihydrochloride), dactolisib (NVP- BEZ235, BEZ-235), dezapelisib, dordaviprone, duvelisib (e.g., a hydrate of duvelisib), eganelisib, fimepinostat, gedatolisib (PF-05212384, PKI-587), idelalisib, inavolisib, leniolisib (e.g., leniolisib phosphate), linperlisib, omipalisib (GSK2126458, GSK458), parsaclisib, pictilisib (GDC-0941), pilaralisib (XL147, SAR245408), paxalisib, rigosertib, risovalisib, seletalisib, serabelisib (TAK-117, MLN1117, INK 1117), sonolisib (PX-866), taselisib (GDC- 0032, RG7604), umbralisib (e.g., umbralisib tosylate), voxtalisib (XL756, SAR245409), wortmannin, zandelisib, AMG 511, AMG319, ASN003, AZD8835, BGT-226 (NVP- BGT226), CH5132799, CUDC-907, GDC-0077, GDC-0084 (RG7666), GS-9820, GSK1059615, GSK2636771, KIN-193 (AZD-6428), LY2023414, LY294002, PF-04691502, PI-103, PKI-402, PQR309, SAR260301, SF1126, SHC-014748-M, TQ-B-3525, VS-5584 (SB2343), WX-037, XL-765, ZSTK474, or a combination thereof. In some embodiments, the PI3K inhibitor is alpelisib, amdizalisib, apitolisib, bimiralisib, buparlisib, copanlisib (e.g., copanlisib dihydrochloride or a hydrate of copanlisib dihydrochloride), dactolisib, dezapelisib, dordaviprone, duvelisib (e.g., a hydrate of duvelisib), eganelisib, fimepinostat, gedatolisib, idelalisib, inavolisib, leniolisib (e.g., leniolisib phosphate), linperlisib, parsaclisib, paxalisib, risovalisib, seletalisib, serabelisib, sonolisib, tenalisib, umbralisib (e.g., umbralisib tosylate), zandelisib, PF-04691502, SHC-014748-M, TQ-B-3525, or a combination thereof. In some embodiments, the Abl inhibitor (e.g., BCR-Abl inhibitor) is asciminib (e.g., asciminib hydrochloride), bafetinib, bosutinib (e.g., bosutinib monohydrate), danusertib, dasatinib (e.g., dasatinib monohydrate), flumatinib (e.g., flumatinib mesylate), imatinib (e.g., imatinib mesylate), nilotinib (e.g., nilotinib monochloride monohydrate), olverembatinib (e.g., olverembatinib mesylate), ponatinib (e.g., ponatinib hydrochloride), radotinib (e.g., radotinib dihydrochloride), risvodetinib (IkT-148009), ruserontinib, vamotinib, vandetanib, AN-019, AT-9283, NPB-001-056, or a combination thereof. In some embodiments, the cancer is a B-ALL, and the additional therapy or therapeutic agent is an Abl inhibitor. In some embodiments, the cancer is a Philadelphia chromosome positive B-ALL and the additional therapy or therapeutic agent is an Abl inhibitor. In some embodiments, the cancer is a Philadelphia chromosome-like B-ALL, and the additional therapy or therapeutic agent is an Abl inhibitor. In some embodiments, the Abl inhibitor is selected from the group consisting of imatinib, dasatinib, ponatinib, or a combination thereof. In some embodiments, the BTK inhibitor is abivertinib, acalabrutinib, atuzabrutinib, branebrutinib, dasatinib (e.g., dasatinib monohydrate), edralbrutinib (SHR-1459), elsubrutinib, evobrutinib, fenebrutinib, ibrutinib, luxeptinib, nemtabrutinib, olafertinib, nemtabrutinib, orelabrutinib, pirtobrutinib, remibrutinib, rilzabrutinib, spebrutinib, sunvozertinib, tirabrutinib (e.g., tirabrutinib hydrochloride), tolebrutinib, vecabrutinib, zanubrutinib, AC-0058 (AC- 0058TA), BMS-986142, CT-1530, DTRMWXHS-12, LY-3337641 (HM-71224), M-7583, TAS-5315, or a combination thereof. In some embodiments, the BTK inhibitor is abivertinib, acalabrutinib, atuzabrutinib, branebrutinib, dasatinib (e.g., dasatinib monohydrate), edralbrutinib, elsubrutinib, evobrutinib, fenebrutinib, ibrutinib, nemtabrutinib, orelabrutinib, pirtobrutinib, remibrutinib, rilzabrutinib, rocbrutinib, spebrutinib, sunvozertinib, tirabrutinib (e.g., tirabrutinib hydrochloride), tolebrutinib, zanubrutinib, AC-0058, BIIB-091, BMS- 986142, DTRMWXHS-12, LY-3337641, TAS-5315, TL-925, or a combination thereof. In some embodiments, the cancer is a B-ALL, and the additional therapy or therapeutic agent is a BTK inhibitor. In some embodiments, the cancer is a pre-BCR+ B-ALL, and the additional therapy or therapeutic agent is a BTK inhibitor. In some embodiments, the cancer is a B-ALL dependent on Ras signaling, and the additional therapy or therapeutic agent is a BTK inhibitor. In some embodiments, the BTK inhibitor is ibrutinib or acalabrutinib. In some embodiments, the JAK inhibitor is abrocitinib, baricitinib, brepocitinib, decernotinib, delgocitinib, deuruxolitinib, elsubrutinib, fedratinib (e.g., fedratinib dihydrochloride monohydrate), filgotinib (e.g., filgotinib maleate), gandotinib, gusacitinib, ilginatinib, itacitinib, ivarmacitinib, izencitinib, jaktinib, momelotinib, nezulcitinib, pacritinib (e.g., pacritinib citrate), peficitinib (e.g., peficitinib hydrobromide), povorcitinib (INCB- 54707), ropsacitinib, ruxolitinib (e.g., ruxolitinib phosphate), solcitinib, tasocitinib (e.g., tofacitinib citrate), tinengotinib, upadacitinib (e.g., upadacitinib hydrate), zasocitinib, AGA- 201, ATI-1777, ATI-501, ESK-001, GLPG-3667, INCB-52793, LNK-01001, LNK-01003, R- 348, TD-8236, TLL-018, TQ-05105, VTX-958, or a combination thereof. In some embodiments, the JAK inhibitor is abrocitinib, baricitinib, brepocitinib, decernotinib, delgocitinib, deuruxolitinib, fedratinib (e.g., fedratinib dihydrochloride monohydrate), filgotinib (e.g., filgotinib maleate), gandotinib, golidocitinib, gusacitinib, ilginatinib, itacitinib, ivarmacitinib, izencitinib, jaktinib, lepzacitinib (ATI-1777), londamocitinib, momelotinib, nezulcitinib, pacritinib (e.g., pacritinib citrate), peficitinib (e.g., peficitinib hydrobromide), povorcitinib (INCB-54707), ritlecitinib (e.g., ritlecitinib tosylate), tasocitinib, ropsacitinib, ruxolitinib (e.g., ruxolitinib phosphate), solcitinib, tofacitinib (e.g., tofacitinib citrate), tinengotinib, upadacitinib (e.g., upadacitinib hydrate), zasocitinib, AGA-201, ATI-501, CPL- 409116, ESK-001, GLPG-3667, LNK-01001, LNK-01003, KL-130008, NS-229, R-348, TD- 8236, TDM-180935, TLL-018, TQ-05105, VC-005, VTX-958, VVN-461, or a combination thereof. In some embodiments, the JAK2 inhibitor is adelatinib, baricitinib, brepocitinib, deuruxolitinib, fedratinib (e.g., fedratinib dihydrochloride monohydrate), filgotinib (e.g., filgotinib maleate), gandotinib, gusacitinib, ilginatinib, izencitinib, jaktinib, momelotinib (e.g., momelotinib dihydrochloride), nezulcitinib, pacritinib (e.g., pacritinib citrate), peficitinib (e.g., peficitinib hydrobromide), ropsacitinib, ruxolitinib (e.g., ruxolitinib phosphate), tasocitinib (e.g., tofacitinib citrate), AT-9283, CPL-409116, KL-130008, TQ-05105, or a combination thereof. In some embodiments, the cancer is a B-ALL, and the additional therapy or therapeutic agent is a JAK inhibitor. In some embodiments, the cancer is a JAK2 (e.g., JAK2R683Gor JAK2I682F) mutant B-ALL, and the additional therapy or therapeutic agent is a JAK inhibitor. In some embodiments, the cancer is a JAK2 (e.g., JAK2R683Gor JAK2I682F) mutant B-ALL with high CRLF2 expression, and the additional therapy or therapeutic agent is a JAK inhibitor (e.g., a JAK2 inhibitor) and a BCL-2 inhibitor (e.g., venetoclax). In some embodiments, the BRaf inhibitor is avutometinib (RO5126766), dabrafenib (e.g., dabrafenib mesylate, GSK2118436), encorafenib (e.g., BRAFTOVI™, LGX818), naporafenib (LXH254), sorafenib (e.g., sorafenib tosylate), vemurafenib (e.g., ZELBORAF®, RO5185426), ARQ-736, AZ304, BMS-908662 (XL281), C17071479-F, CHIR-265 (RAF265), FORE-8394 (PLX-8394), GDC-0879, GDC-5573 (HM95573), HLX-208, PLX- 3603, PLX-4720, or a combination thereof. In some embodiments, the BRaf inhibitor is avutometinib, dabrafenib (e.g., dabrafenib mesylate), encorafenib, naporafenib, sorafenib (e.g., sorafenib tosylate), vemurafenib, C17071479-F, CHIR-265, FORE-8394, HLX-208, or a combination thereof. In some embodiments, the MEK inhibitor is avutometinib, binimetinib, cobimetinib (e.g., cobimetinib fumarate), mirdametinib, nedometinib, pimasertib, refametinib, selumetinib (e.g., selumetinib sulfate), trametinib (e.g., trametinib dimethyl sulfoxide, GSK-1120212), tunlametinib, zapnometinib, FCN-159, NFX-179, TAK-733, or a combination thereof. In some embodiments, the MEK inhibitor is a MEK-Raf protein-protein interaction stabilizer, such as NST-628 or avutometinib (VS6766). In some embodiments, the menin inhibitor is revumenib (e.g., revumenib fumarate), icovamenib (BMF-219), ziftomenib, DS-1594, DSP-5336, HMPL-506, JNJ-6617, or a combination thereof. In some embodiments, the cancer is a B-ALL, and the additional therapy or therapeutic agent is a menin inhibitor. In some embodiments, the cancer is an MLL-rearranged (e.g., an MLL-Af4 fusion, an MLL-Af6 fusion, an MLL-Af9 fusion, an MLL-ENL fusion, or an MLL- PTD fusion) B-ALL, and the additional therapy or therapeutic agent is a menin inhibitor. In some embodiments, the BCL-2 inhibitor is foselutoclax (UBX-1325), lacutoclax, lisaftoclax, navitoclax, obatoclax, pelcitoclax, venetoclax, sonrotoclax (BGB-11417), surzetoclax, oblimersen (e.g., oblimersen sodium), beclanorsen, AZD-0466, ICP-248, TQB- 3909, UBX-1967, ZN-d5, or a combination thereof. In some embodiments, the BCL-2 inhibitor is foselutoclax (UBX-1325), lisaftoclax, navitoclax, obatoclax, pelcitoclax, venetoclax, sonrotoclax, oblimersen (e.g., oblimersen sodium), beclanorsen, or a combination thereof. In some embodiments, the cancer is a B-ALL, and the additional therapy or therapeutic agent is a BCL-2 inhibitor. In some embodiments, the cancer is an MLL-rearranged (e.g., an MLL-Af4 fusion, an MLL-Af6 fusion, an MLL-Af9 fusion, an MLL-ENL fusion, or an MLL- PTD fusion) B-ALL, and the additional therapy or therapeutic agent is a BCL-2 inhibitor. In some embodiments, the cancer is a BCL2 amplified B-ALL, and the additional therapy or therapeutic agent is a BCL-2 inhibitor. In some embodiments, the BCL-2 inhibitor is venetoclax. In some embodiments, the cancer is a large B cell lymphoma (e.g., diffuse large B-cell lymphoma not otherwise specified (DLBCL-NOS), diffuse large B-cell lymphoma / high grade B cell lymphoma (HGBCL) (e.g., HGBCL with MYC and / or BCL2 rearrangements (HGBCL- MYC / BCL-2)), primary large B cell lymphoma of immune-privileged sites (primary LBCL of immune-privileged sites), intravascular large B-cell lymphoma (IVLBCL), primary mediastinal large B cell lymphoma (primary mediastinal LBCL), or high grade B-cell lymphoma NOS (HBGCL-NOS)), follicular lymphoma (FL), mantle cell lymphoma (MCL), or a transformation of an indolent B cell lymphoma, and the additional therapy or therapeutic agent is a BCL-2 inhibitor. In some embodiments, the cancer is a large B cell lymphoma (e.g., diffuse large B-cell lymphoma not otherwise specified (DLBCL-NOS), diffuse large B-cell lymphoma / high grade B cell lymphoma (HGBCL) (e.g., HGBCL with MYC and / or BCL2 rearrangements (HGBCL-MYC / BCL-2)), primary large B cell lymphoma of immune- privileged sites (primary LBCL of immune-privileged sites), intravascular large B-cell lymphoma (IVLBCL), primary mediastinal large B cell lymphoma (primary mediastinal LBCL), or high grade B-cell lymphoma NOS (HBGCL-NOS)), and the additional therapy or therapeutic agent is a BCL-2 inhibitor. In some embodiments, the cancer is a transformation of an indolent B cell lymphoma, and the additional therapy or therapeutic agent is a BCL-2 inhibitor. In some embodiments, the cancer is a DLBCL-NOS, and the additional therapy or therapeutic agent is a BCL-2 inhibitor. In some embodiments, the BCL-2 inhibitor is venetoclax. In some embodiments, the cancer is a FL, and the additional therapy or therapeutic agent is a BCL-2 inhibitor. In some embodiments, the BCL-2 inhibitor is venetoclax. In some embodiments, the cancer is an MCL, and the additional therapy or therapeutic agent is a BCL-2 inhibitor. In some embodiments, the BCL-2 inhibitor is venetoclax. In some embodiments, the cancer is a T-ALL, and the additional therapy or therapeutic agent is a BCL-2 inhibitor. In some embodiments, the BCL-2 inhibitor is venetoclax. In some embodiments, the BCL-XL inhibitor is lisaftoclax, navitoclax, obatoclax, pelcitoclax, mirzotamab clezutoclax, ABBV-155, APG-1252-12A, AZD-0466, DT-2216, PA- 15227, UBX-1325, UBX-1967, XZ-739, 753-B, or a combination thereof. In some embodiments, the BCL-XL inhibitor is lisaftoclax, navitoclax, obatoclax, or a combination thereof. In some embodiments, the MCL-1 inhibitor or degrader is omacetaxine (e.g., omacetaxine mepesuccinate), murizatoclax, tapotoclax, ABBV-467, GS-9716 S-64315, or a combination thereof. In some embodiments, the XPO1 inhibitor is eltanexor, felezonexor, selinexor, verdinexor, BIIB-100, JS-110, or a combination thereof. In some embodiments, the XPO1 inhibitor is selinexor. In some embodiments, the inhibitor of the PRC2 is lirametostat, mevrometostat, tazemetostat (e.g., tazemetostat hydrobromide), valemetostat (e.g., valemetostat tosylate), tulmimetostat (CPI-0209), EBI-2511, HH-2853, HM-97662, SHR-2554, XNW-5004, or a combination thereof. In some embodiments, the inhibitor of the PRC2 is an EZH1 / 2 inhibitor. In some embodiments, the EZH1 / 2 inhibitor is valemetostat (e.g., valemetostat tosylate), tulmimetostat (CPI-0209), HH-2853, HM-97662, or a combination thereof. In some embodiments, the inhibitor of the PRC2 is an EZH2 inhibitor. In some embodiments, the EZH2 inhibitor is lirametostat, mevrometostat, tazemetostat (e.g., tazemetostat hydrobromide), EBI- 2511, SHR-2554, XNW-5004, or a combination thereof. Non-limiting examples of EZH2 and / or EZH1 / 2 inhibitors are described in International Publication Nos. WO 2011 / 140325, WO 2012 / 005805, WO 2012 / 050532, WO 2012 / 118812, WO 2012 / 142513, WO 2012 / 142504, WO 2013 / 049770, WO 2013 / 039988, WO 2013 / 067300, WO 2015 / 141616, WO 2017 / 084494, WO 2018 / 210296, WO 2018 / 210302, WO 2019 / 091450, WO 2019 / 204490, WO 2019 / 226491, WO 2020 / 063863, WO 2020 / 171606, WO 2020 / 228591, WO 2021 / 016414, WO 2021 / 063332, WO 2021 / 063340, WO 2021 / 180235, and WO 2022 / 035303. In some embodiments, the cancer is a large B cell lymphoma (e.g., diffuse large B-cell lymphoma not otherwise specified (DLBCL-NOS), diffuse large B-cell lymphoma / high grade B cell lymphoma (HGBCL) (e.g., HGBCL with MYC and / or BCL2 rearrangements (HGBCL- MYC / BCL-2)), primary large B cell lymphoma of immune-privileged sites (primary LBCL of immune-privileged sites), intravascular large B-cell lymphoma (IVLBCL), primary mediastinal large B cell lymphoma (primary mediastinal LBCL), or high grade B-cell lymphoma NOS (HBGCL-NOS)), follicular lymphoma (FL), mantle cell lymphoma (MCL), or a transformation of an indolent B cell lymphoma, and the additional therapy or therapeutic agent is an inhibitor of the PRC2 (e.g., an EZH1 / 2 or EZH2 inhibitor). In some embodiments, the cancer is a large B cell lymphoma (e.g., diffuse large B-cell lymphoma not otherwise specified (DLBCL-NOS), diffuse large B-cell lymphoma / high grade B cell lymphoma (HGBCL) (e.g., HGBCL with MYC and / or BCL2 rearrangements (HGBCL-MYC / BCL-2)), primary large B cell lymphoma of immune-privileged sites (primary LBCL of immune- privileged sites), intravascular large B-cell lymphoma (IVLBCL), primary mediastinal large B cell lymphoma (primary mediastinal LBCL), or high grade B-cell lymphoma NOS (HBGCL- NOS)), and the additional therapy or therapeutic agent is an inhibitor of the PRC2 (e.g., an EZH1 / 2 or EZH2 inhibitor). In some embodiments, the cancer is a DLBCL-NOS, and the additional therapy or therapeutic agent is an inhibitor of the PRC2 (e.g., an EZH1 / 2 or EZH2 inhibitor). In some embodiments, the cancer is a diffuse large B-cell lymphoma / high grade B cell lymphoma (HGBCL) (e.g., HGBCL with MYC and / or BCL2 rearrangements (HGBCL- MYC / BCL-2)), and the additional therapy or therapeutic agent is an inhibitor of the PRC2 (e.g., an EZH1 / 2 or EZH2 inhibitor). In some embodiments, the cancer is a HBGCL-NOS, and the additional therapy or therapeutic agent is an inhibitor of the PRC2 (e.g., an EZH1 / 2 or EZH2 inhibitor). In some embodiments, the cancer is a primary mediastinal large B cell lymphoma, and the additional therapy or therapeutic agent is an inhibitor of the PRC2 (e.g., an EZH1 / 2 or EZH2 inhibitor). In some embodiments, the cancer is a primary large B cell lymphoma of immune-privileged sites (primary LBCL of immune-privileged sites), and the additional therapy or therapeutic agent is an inhibitor of the PRC2 (e.g., an EZH1 / 2 or EZH2 inhibitor). In some embodiments, the cancer is a follicular lymphoma (FL), and the additional therapy or therapeutic agent is an inhibitor of the PRC2 (e.g., an EZH1 / 2 or EZH2 inhibitor). In some embodiments, the cancer is a mantle cell lymphoma (MCL), and the additional therapy or therapeutic agent is an inhibitor of the PRC2 (e.g., an EZH1 / 2 or EZH2 inhibitor). In some embodiments, the cancer is a transformation of an indolent B cell lymphoma, and the additional therapy or therapeutic agent is an inhibitor of the PRC2 (e.g., an EZH1 / 2 or EZH2 inhibitor). In some embodiments, the cancer is a BL, and the additional therapy or therapeutic agent is an inhibitor of the PRC2 (e.g., an EZH1 / 2 or EZH2 inhibitor). In some embodiments, the cancer is a NLPHL, and the additional therapy or therapeutic agent is an inhibitor of the PRC2 (e.g., an EZH1 / 2 or EZH2 inhibitor). In some embodiments, the cancer is a B-ALL (e.g., Philadelphia chromosome positive B-ALL, Philadelphia chromosome negative B-ALL, or B-ALL with an MLL rearrangement (e.g., an MLL-Af4 fusion, an MLL-Af6 fusion, an MLL-Af9 fusion, an MLL-ENL fusion, or an MLL-PTD fusion)), and the additional therapy or therapeutic agent is an inhibitor of the PRC2. In some embodiments, the cancer is a FL, and the additional therapy or therapeutic agent is an inhibitor of the PRC2 (e.g., an EZH1 / 2 or EZH2 inhibitor). In some embodiments, the cancer is an MCL, and the additional therapy or therapeutic agent is an inhibitor of the PRC2 (e.g., an EZH1 / 2 or EZH2 inhibitor). In some embodiments, the cancer is peripheral T-cell lymphoma (PTCL) (e.g., anaplastic large cell lymphoma (ALCL) (e.g., ALK-positive anaplastic large cell lymphoma, or ALK-negative anaplastic large cell lymphoma), nodal T follicular helper cell lymphoma (e.g., nodal T follicular helper cell lymphoma angioimmunoblastic type (also known as angioimmunoblastic T-cell lymphoma (AITL) or follicular helper T-cell lymphoma, angioimmunoblastic type), nodal T follicular helper cell lymphoma follicular type (also known as follicular helper T-cell lymphoma, follicular type), or nodal T follicular helper cell lymphoma NOS (also known as follicular helper T-cell lymphoma, NOS))), or a primary cutaneous T-cell lymphoid proliferation or lymphoma (cutaneous T-cell lymphoma (CTCL)) (e.g., primary cutaneous CD4-positive small or medium T-cell lymphoproliferative disorder, mycosis fungoides, Sezary syndrome, or primary cutaneous gamma-delta T-cell lymphoma), and the additional therapy or therapeutic agent is an inhibitor of the PRC2 (e.g., an EZH1 / 2 or EZH2 inhibitor). In some embodiments, the cancer is peripheral T-cell lymphoma (PTCL) (e.g., anaplastic large cell lymphoma (ALCL) (e.g., ALK-positive anaplastic large cell lymphoma, or ALK-negative anaplastic large cell lymphoma), nodal T follicular helper cell lymphoma (e.g., nodal T follicular helper cell lymphoma angioimmunoblastic type (also known as angioimmunoblastic T-cell lymphoma (AITL) or follicular helper T-cell lymphoma, angioimmunoblastic type), nodal T follicular helper cell lymphoma follicular type (also known as follicular helper T-cell lymphoma, follicular type), or nodal T follicular helper cell lymphoma NOS (also known as follicular helper T-cell lymphoma, NOS))), and the additional therapy or therapeutic agent is an inhibitor of the PRC2 (e.g., an EZH1 / 2 or EZH2 inhibitor). In some embodiments, the cancer is anaplastic large cell lymphoma (ALCL) (e.g., ALK- positive anaplastic large cell lymphoma, or ALK-negative anaplastic large cell lymphoma), and the additional therapy or therapeutic agent is an inhibitor of the PRC2 (e.g., an EZH1 / 2 or EZH2 inhibitor). In some embodiments, the cancer is ALK-positive anaplastic large cell lymphoma, and the additional therapy or therapeutic agent is an inhibitor of the PRC2 (e.g., an EZH1 / 2 or EZH2 inhibitor). In some embodiments, the cancer is ALK-negative anaplastic large cell lymphoma, and the additional therapy or therapeutic agent is an inhibitor of the PRC2 (e.g., an EZH1 / 2 or EZH2 inhibitor). In some embodiments, the cancer is nodal T follicular helper cell lymphoma (e.g., nodal T follicular helper cell lymphoma angioimmunoblastic type (also known as angioimmunoblastic T-cell lymphoma (AITL) or follicular helper T-cell lymphoma, angioimmunoblastic type), nodal T follicular helper cell lymphoma follicular type (also known as follicular helper T-cell lymphoma, follicular type), or nodal T follicular helper cell lymphoma NOS (also known as follicular helper T-cell lymphoma, NOS)), and the additional therapy or therapeutic agent is an inhibitor of the PRC2 (e.g., an EZH1 / 2 or EZH2 inhibitor). In some embodiments, the cancer is nodal T follicular helper cell lymphoma angioimmunoblastic type (also known as angioimmunoblastic T-cell lymphoma (AITL) or follicular helper T-cell lymphoma, angioimmunoblastic type), and the additional therapy or therapeutic agent is an inhibitor of the PRC2 (e.g., an EZH1 / 2 or EZH2 inhibitor). In some embodiments, the cancer is nodal T follicular helper cell lymphoma follicular type (also known as follicular helper T-cell lymphoma, follicular type), and the additional therapy or therapeutic agent is an inhibitor of the PRC2 (e.g., an EZH1 / 2 or EZH2 inhibitor). In some embodiments, the cancer is nodal T follicular helper cell lymphoma NOS (also known as follicular helper T- cell lymphoma, NOS), and the additional therapy or therapeutic agent is an inhibitor of the PRC2 (e.g., an EZH1 / 2 or EZH2 inhibitor). In some embodiments, the cancer is a primary cutaneous T-cell lymphoid proliferation or lymphoma (cutaneous T-cell lymphoma (CTCL)) (e.g., primary cutaneous CD4-positive small or medium T-cell lymphoproliferative disorder, mycosis fungoides, Sezary syndrome, or primary cutaneous gamma-delta T-cell lymphoma), and the additional therapy or therapeutic agent is an inhibitor of the PRC2 (e.g., an EZH1 / 2 or EZH2 inhibitor). In some embodiments, the cancer is mycosis fungoides, and the additional therapy or therapeutic agent is an inhibitor of the PRC2 (e.g., an EZH1 / 2 or EZH2 inhibitor). In some embodiments, the cancer is Sezary syndrome, and the additional therapy or therapeutic agent is an inhibitor of the PRC2 (e.g., an EZH1 / 2 or EZH2 inhibitor). An exemplary wild-type human EZH2 sequence is shown below. This is one of several isoforms of EZH2, and it will be understood that residue numbering can change based on the reference isoform. SEQ ID NO: 1 (UniParc ID UPI000006D77C): In some embodiments, the steroid is dexamethasone, prednisone, or a combination thereof. In some embodiments, the immunomodulatory imide drug is avadomide, lenalidomide, iberdomide, pomalidomide, thalidomide, CC-99282, or a combination thereof. In some embodiments, the additional therapy or therapeutic agent is lenalidomide and rituximab or obinutuzumab. In some embodiments, the anti-CD19 therapy is blinatumomab (e.g., BLINCYTO® (blinatumomab) or a biosimilar thereof), coltuximab ravtansine, inebilizumab (e.g., inebilizumab-cdon, or a biosimilar thereof), loncastuximab tesirine (e.g., loncastuximab tesirine-lpyl, or a biosimilar thereof), obexelimab, tafasitamab (e.g., tafasitamab-cxix, or a biosimilar thereof), dDT-2219, LY-3541860, biosimilars thereof, or a combination thereof. In some embodiments, the anti-CD19 therapy is a bispecific antibody or antigen-binding fragment thereof (e.g., BLINCYTO® (blinatumomab) or a biosimilar thereof). In some embodiments, the anti-CD19 therapy is an anti-CD19 and anti-CD3 bispecific antibody or antigen-binding fragment thereof (e.g., BLINCYTO® (blinatumomab) or a biosimilar thereof). In some embodiments, the anti-CD19 therapy is an antibody-drug conjugate (e.g., coltuximab ravtansine, loncastuximab tesirine (e.g., loncastuximab tesirine-lpyl, or a biosimilar thereof), or a biosimilar thereof). In some embodiments, the anti-CD20 therapy is divozilimab, epcoritamab (e.g., epcoritamab-bysp, or a biosimilar thereof), glofitamab (e.g., COLUMVI® (glofitamab), or a biosimilar thereof), ibritumomab tiuxetan (e.g., ZEVALIN® (ibritumomab tiuxetan), or a biosimilar thereof), mosunetuzumab (e.g., mosunetuzumab-axgb, or a biosimilar thereof), obinutuzumab (e.g., GAZYVA® (obinutuzumab), or a biosimilar thereof), ocrelizumab (e.g., OCREVUS® (ocrelizumab), or a biosimilar thereof), odronextamab, ofatumumab (e.g., ARZERRA® (ofatumumab), or a biosimilar thereof), plamotamab, rituximab (e.g., RITUXAN® (rituximab), or a biosimilar thereof (e.g., rituximab-abbs, rituximab-arrx, rituximab-pvvr, ACELLBIA® (rituximab), HALPRYZA® (rituximab), HANLIKON® (rituximab), RIXATHON® (rituximab), REDITUX™ (rituximab), Retuxira (rituximab), BI- 695500, GB-241, Mabion-CD20, RTXM-83, SAIT-101), ublituximab (e.g., ublituximab-xiiy, or a biosimilar thereof), veltuzumab, zuberitamab, MIL-62, SCT-400, TQB-2303, biosimilars thereof, or a combination thereof. In some embodiments, the anti-CD20 therapy is a bispecific antibody or antigen-binding fragment thereof (e.g., epcoritamab (e.g., epcoritamab-bysp, or a biosimilar thereof), glofitamab (e.g., COLUMVI® (glofitamab), or a biosimilar thereof), mosunetuzumab (e.g., mosunetuzumab-axgb, or a biosimilar thereof), plamotamab, odronextamab, biosimilars thereof, or a combination thereof. In some embodiments, the anti- CD20 therapy is an anti-CD20 and anti-CD3 bispecific antibody or antigen-binding fragment thereof (e.g., epcoritamab (e.g., epcoritamab-bysp, or a biosimilar thereof), glofitamab (e.g., COLUMVI® (glofitamab), or a biosimilar thereof), mosunetuzumab (e.g., mosunetuzumab- axgb, or a biosimilar thereof), plamotamab, odronextamab, biosimilars thereof, or a combination thereof. In some embodiments, the anti-CD20 therapy is an antibody-drug conjugate (e.g., ibritumomab tiuxetan (e.g., ZEVALIN® (ibritumomab tiuxetan), or a biosimilar thereof). In some embodiments, the additional therapy or therapeutic agent is rituximab. In some such embodiments, the combination of rituximab and a compound provided herein, or a pharmaceutically acceptable salt thereof, is used as maintenance therapy. In some such embodiments, the cancer is a FL. In some embodiments, the additional therapy or therapeutic agent is obinutuzumab. In some such embodiments, the combination of obinutuzumab and a compound provided herein, or a pharmaceutically acceptable salt thereof, is used as maintenance therapy. In some such embodiments, the cancer is a FL. In some embodiments, the cancer is a large B cell lymphoma (e.g., diffuse large B-cell lymphoma not otherwise specified (DLBCL-NOS), diffuse large B-cell lymphoma / high grade B cell lymphoma (HGBCL) (e.g., HGBCL with MYC and / or BCL2 rearrangements (HGBCL- MYC / BCL-2)), primary large B cell lymphoma of immune-privileged sites (primary LBCL of immune-privileged sites), intravascular large B-cell lymphoma (IVLBCL), primary mediastinal large B cell lymphoma (primary mediastinal LBCL), or high grade B-cell lymphoma NOS (HBGCL-NOS)), follicular lymphoma (FL), mantle cell lymphoma (MCL), or transformations of indolent B cell lymphomas, and the additional therapy or therapeutic agent is anti-CD20 therapy. In some embodiments, the cancer is a large B cell lymphoma (e.g., diffuse large B-cell lymphoma not otherwise specified (DLBCL-NOS), diffuse large B-cell lymphoma / high grade B cell lymphoma (HGBCL) (e.g., HGBCL with MYC and / or BCL2 rearrangements (HGBCL-MYC / BCL-2)), primary large B cell lymphoma of immune- privileged sites (primary LBCL of immune-privileged sites), intravascular large B-cell lymphoma (IVLBCL), primary mediastinal large B cell lymphoma (primary mediastinal LBCL), or high grade B-cell lymphoma NOS (HBGCL-NOS)), and the additional therapy or therapeutic agent is anti-CD20 therapy. In some embodiments, the cancer is mantle cell lymphoma (MCL), and the additional therapy or therapeutic agent is anti-CD20 therapy. In some embodiments, the cancer is a transformation of an indolent B cell lymphoma, and the additional therapy or therapeutic agent is anti-CD20 therapy. In some embodiments, the anti- CD20 therapy is rituximab, obinutuzumab, or a combination thereof. In some embodiments, the cancer is a FL, and the additional therapy or therapeutic agent is anti-CD20 therapy. In some embodiments, the anti-CD20 therapy is rituximab, obinutuzumab, or a combination thereof. In some embodiments, the anti-CD22 therapy is bectumomab, epratuzumab, inotuzumab ozogamicin (e.g., BESPONSA® (inotuzumab ozogamicin), or a biosimilar thereof), moxetumomab pasudotox (e.g., LUMOXITI® (moxetumomab pasudotox), or a biosimilar thereof), pinatuzumab vedotin, suciraslimab, dDT-2219, biosimilars thereof, or a combination thereof. In some embodiments, the anti-CD22 therapy is an antibody-drug conjugate (e.g., inotuzumab ozogamicin (e.g., BESPONSA® (inotuzumab ozogamicin), or a biosimilar thereof), pinatuzumab vedotin, dDT-2219, biosimilars thereof, or a combination thereof. In some embodiments, the anti-CD22 therapy is an immunotoxin (e.g., moxetumomab pasudotox (e.g., LUMOXITI® (moxetumomab pasudotox), or a biosimilar thereof)). In some embodiments, the anti-CD22 therapy is inotuzumab ozogamicin. In some embodiments, the cancer is a B-ALL, and the additional therapy or therapeutic agent is anti-CD22 therapy. In some embodiments, the anti-CD22 therapy is an anti-CD22 antibody-drug conjugate (e.g., inotuzumab ozogamicin, or a biosimilar thereof). In some embodiments, the anti-CD3 therapy is blinatumomab (e.g., BLINCYTO® (blinatumomab), or a biosimilar thereof), catumaxomab, elranatamab, epcoritamab, ertumaxomab, glofitamab (e.g., COLUMVI® (glofitamab), or a biosimilar thereof), linvoseltamab, mosunetuzumab (e.g., mosunetuzumab-axgb, or a biosimilar thereof), odronextamab, otelixizumab, plamotamab, talquetamab, tarlatamab, tebentafusp (e.g., tebentafusp-tebn, or a biosimilar thereof), teclistamab (e.g., teclistamab-cqyv, or a biosimilar thereof), teplizumab (e.g., teplizumab-mzwv, or a biosimilar thereof), visilizumab, biosimilars thereof, or a combination thereof. In some embodiments, the anti-CD3 therapy is bispecific antibody or antigen-binding fragment thereof (e.g., blinatumomab (e.g., BLINCYTO® (blinatumomab), or a biosimilar thereof), catumaxomab, elranatamab, epcoritamab (e.g., epcoritamab-bysp, or a biosimilar thereof), ertumaxomab, glofitamab (e.g., COLUMVI® (glofitamab), or a biosimilar thereof), linvoseltamab, mosunetuzumab (e.g., mosunetuzumab- axgb, or a biosimilar thereof), plamotamab, odronextamab, talquetamab, tarlatamab, tebentafusp (e.g., tebentafusp-tebn, or a biosimilar thereof), teclistamab (e.g., teclistamab- cqyv, or a biosimilar thereof), biosimilars thereof, or a combination thereof. In some embodiments, the anti-CD3 therapy is an anti-CD3 and anti-CD19 bispecific antibody or antigen-binding fragment thereof (e.g., BLINCYTO® (blinatumomab) or a biosimilar thereof). In some embodiments, the anti-CD3 therapy is an anti-CD20 and anti-CD3 bispecific antibody or antigen-binding fragment thereof (e.g., epcoritamab (e.g., epcoritamab-bysp, or a biosimilar thereof), glofitamab (e.g., COLUMVI® (glofitamab), or a biosimilar thereof), mosunetuzumab (e.g., mosunetuzumab-axgb, or a biosimilar thereof), plamotamab, odronextamab, biosimilars thereof, or a combination thereof. In some embodiments, the anti-CD30 therapy is acimtamig, brentuximab, brentuximab vedotin (e.g., ADCETRIS®, or a biosimilar thereof), iratumumab, biosimilars thereof, or a combination thereof. In some embodiments, the anti-CD30 therapy is a bispecific antibody or antigen-binding fragment thereof (e.g., acimtamig), or a biosimilar thereof. In some embodiments, the anti-CD30 therapy is an antibody-drug conjugate (e.g., brentuximab vedotin (e.g., ADCETRIS®, or a biosimilar thereof), or a biosimilar thereof. In some embodiments, the anti-CD79B therapy is polatuzumab (e.g., polatuzumab vedotin (e.g., polatuzumab vedotin-piiq, or a biosimilar thereof)), MGD-010, RG-7986, biosimilars thereof, or a combination thereof. In some embodiments, the anti-CD79B therapy is polatuzumab (e.g., polatuzumab vedotin (e.g., polatuzumab vedotin-piiq, or a biosimilar thereof)), MGD-010, biosimilars thereof, or a combination thereof. In some embodiments, the anti-CD79B therapy is a bispecific antibody or antigen-binding fragment thereof (e.g., MGD- 010). In some embodiments, the anti-CD79B therapy is an antibody-drug conjugate (e.g., polatuzumab vedotin (e.g., polatuzumab vedotin-piiq, or a biosimilar thereof)). In some embodiments, the anti-PD1 therapy is balstilimab, budig...

Claims

WHAT IS CLAIMED IS:

1. A compound of Formula (I-c):Formula (I-c) or a pharmaceutically acceptable salt thereof, wherein: m3 is 1; X3is C1-3alkylene; R1is H; R2ais H; R5is selected from the group consisting of: -OH, -NH2, -R5A, -OR5A, and -NR5ARf, wherein: R5Ais selected from the group consisting of: C1-6 alkyl optionally substituted with 1-3 Rc; and -(C0-3 alkylene)-Rb1, wherein the C0-3 alkylene is optionally substituted with 1-2 Rc; Xais selected from the group consisting of: N and CRXa; R6and RXaare independently selected from the group consisting of: H, halo, C1-2 alkyl, C1-2haloalkyl, C1-2alkoxy, CN, and -C≡CH; m4 and m5 are independently 0, 1, or 2; each Ra4and Ra5is independently selected from the group consisting of: -F, CN, C1-3alkoxy, OH, and C1-3 alkyl optionally substituted with 1-3 F; LA1is CH2 or CHRL, wherein RLis selected from the group consisting of: -F, -OH, and C1-3alkyl optionally substituted with 1-3 Rc(e.g., C1-3alkyl optionally substituted with 1-3 -F);c1 is 0, 1, or 2; RYais C1-6 alkyl optionally substituted with 1-3 Rc; each RYbis independently selected from the group consisting of: -F and C1-3alkyl optionally substituted with 1-3 -F; X is CH; each Rb1is independently selected from the group consisting of: C3-6 cycloalkyl and 4- 8 membered heterocyclyl, each of which is optionally substituted with 1-3 Rg; each Rcis independently selected from the group consisting of: halo, cyano, -OH, -C1- 6 alkoxy, -C1-6 haloalkoxy, -NRdRe, C(=O)C1-6 alkyl, C(=O)OC1-6 alkyl, C(=O)N(Rf)2, S(O)0-2(C1-6alkyl), and S(O)0-2(C1-6haloalkyl); each Rdand Reis independently selected from the group consisting of: H, C(=O)C1-6alkyl, C(=O)C1-6 haloalkyl, C(=O)OC1-6 alkyl, C(=O)OC1-6 haloalkyl, C(=O)N(Rf)2, S(O)1- 2(C1-6 alkyl), S(O)1-2(C1-6 haloalkyl), S(O)1-2N(Rf)2, and C1-6 alkyl optionally substituted with 1-3 Rh; each Rfis independently selected from the group consisting of: H and C1-6 alkyl optionally substituted with 1-3 Rh; each Rgis independently selected from the group consisting of: Rh, oxo, C1-3alkyl, and C1-3 haloalkyl; and each Rhis independently selected from the group consisting of: halo, cyano, -OH, -(C0-3alkylene)-C1-6alkoxy, -(C0-3alkylene)-C1-6haloalkoxy, -(C0-3alkylene)-NH2, -(C0-3alkylene)-N(H)(C1-3alkyl), and –(C0-3alkylene)-N(C1-3alkyl)2.

2. The compound of claim 1, wherein the compound is other than Compound Nos. R242, R242a, R242b, R212, or R167, as depicted in Table R1, or a pharmaceutically acceptable salt thereof.

3. The compound of claim 1, wherein one or more of (1)-(3) applies: (1) m4 is 1 or 2, wherein each Ra4is independently C1-3 alkyl optionally substituted with 1-3 F; (2) m5 is 1 or 2; and / or (3) c1 is 1 or 2.

4. The compound of any one of claims 1-3, wherein m4 is 0; and m5 is 0.

5. The compound of any one of claims 1-3, wherein m4 is 1 or 2, wherein each Ra4is independently C1-3 alkyl optionally substituted with 1-3 F; and m5 is 0.

6. The compound of any one of claims 1-5, wherein LA1is CH2.

7. The compound of any one of claims 1-4, wherein the8. The compound of any one of claims 1-3 or 5-6, wherein the).

9. The compound of any one of claims 1-8, wherein c1 is 0.

10. The compound of any one of claims 1-8, wherein c1 is 1 or 2.

11. The compound of any one of claims 1-8 or 10, wherein themoiety is selected from the group consisting of:, ,.

12. The compound of any one of claims 1-11, wherein RYais methyl.

13. The compound of any one of claims 1-12, wherein each RYbis -F.

14. The compound of any one of claims 1-13, wherein R5is -NR5ARf.

15. The compound of any one of claims 1-14, wherein R5is -NH(Me).

16. The compound of any one of claims 1-15, wherein –(X3)m3-R1is isopropyl.

17. The compound of any one of claims 1-16, wherein R6is -Cl.

18. The compound of any one of claims 1-17, wherein Xais N.

19. The compound of any one of claims 1-13, wherein R5is -NH(Me); R6is -Cl; and Xais N.

20. The compound of claim 1, wherein the compound of Formula (I-c) is selected from the group consisting of the Compound Nos.109, 119, 120, 126, 126a, 126b, 127, 127a, 127b, 128, 129, 129a, 129b, 130, 130a, 130b, 133, 134, 138, 138a, 138b, 139, 139a, 139b, 140, 140a, and 140b, as depicted in Table C1, or a pharmaceutically acceptable salt thereof.

21. The compound of claim 1, wherein the compound of Formula (I-c) is selected from the group consisting of: 2-[[6-[[5-chloro-2-[(3S,4S)-4-[[4-[3-(2,6-dioxo-3-piperidyl)-5-fluoro-1-methyl- indazol-6-yl]-1-piperidyl]methyl]-3-methyl-1-piperidyl]pyrimidin-4-yl]amino]-1-isopropyl- 2-oxo-1,8-naphthyridin-3-yl]oxy]-N-methyl-acetamide; 2-((6-((5-chloro-2-(4-((4-(3-(2,6-dioxopiperidin-3-yl)-5-fluoro-1-methyl-1H-indazol- 6-yl)piperidin-1-yl)methyl)piperidin-1-yl)pyrimidin-4-yl)amino)-1-isopropyl-2-oxo-1,2- dihydro-1,8-naphthyridin-3-yl)oxy)-N-methylacetamide; and 2-((6-((5-chloro-2-(4-((4-(3-(2,6-dioxopiperidin-3-yl)-7-fluoro-1-methyl-1H-indazol- 6-yl)piperidin-1-yl)methyl)piperidin-1-yl)pyrimidin-4-yl)amino)-1-isopropyl-2-oxo-1,2- dihydro-1,8-naphthyridin-3-yl)oxy)-N-methylacetamide, or a pharmaceutically acceptable salt thereof.

22. A pharmaceutical composition comprising a compound of any one of claims 1- 21, or a pharmaceutically acceptable salt thereof, and a pharmaceutically acceptable excipient.

23. A method for treating a cancer in a subject in need thereof, the method comprising administering to the subject a therapeutically effective amount of a compound of any one of claims 1-21, or a pharmaceutically acceptable salt thereof, or a pharmaceutical composition according to claim 22.

24. The method of claim 23, wherein the cancer is a hematological cancer, breast cancer, gastrointestinal cancer, brain cancer, lung cancer, or a combination thereof.

25. The method of claim 24, wherein the cancer is a hematological cancer (e.g., lymphoma (e.g., Hodgkin lymphoma (e.g., nodular lymphocyte predominant Hodgkin lymphoma (NLPHL)), non-Hodgkin lymphoma (e.g., B cell lymphoid proliferations and lymphomas (e.g., mature B cell neoplasms (e.g., Burkitt lymphoma (BL), large B cell lymphoma (e.g., diffuse large B-cell lymphoma not otherwise specified (DLBCL-NOS), T- cell / histiocyte-rich large B-cell lymphoma, diffuse large B-cell lymphoma / high grade B cell lymphoma (HGBCL) (e.g., HGBCL with MYC and / or BCL2 rearrangements (HGBCL- MYC / BCL-2)), primary large B cell lymphoma of immune-privileged sites (primary LBCL of immune-privileged sites), primary mediastinal large B cell lymphoma (primary mediastinal LBCL), or high grade B-cell lymphoma NOS), follicular lymphoma (FL), or transformationsof indolent B cell lymphomas)), T-cell and NK-cell lymphoid proliferations and lymphomas (e.g., mature T-cell and NK-cell neoplasms (e.g., mature T-cell and NK-cell leukemias (e.g., adult T-cell leukemia / lymphoma), primary cutaneous T-cell lymphoid proliferations and lymphomas (cutaneous T-cell lymphoma (CTCL)) (e.g., primary cutaneous CD4-positive small or medium T-cell lymphoproliferative disorder, mycosis fungoides, Sezary syndrome, primary cutaneous CD30-positive T-cell lymphoproliferative disorder: lymphomatoid papulosis, primary cutaneous CD30-positive T-cell lymphoproliferative disorder: primary cutaneous anaplastic large cell lymphoma, subcutaneous panniculitis-like T-cell lymphoma, primary cutaneous gamma-delta T-cell lymphoma, or primary cutaneous peripheral T-cell lymphoma NOS), peripheral T-cell lymphoma (PTCL) (e.g., anaplastic large cell lymphoma (ALCL) (e.g., ALK-positive anaplastic large cell lymphoma, or ALK-negative anaplastic large cell lymphoma), nodal T follicular helper cell lymphoma (e.g., nodal T follicular helper cell lymphoma angioimmunoblastic type (also known as angioimmunoblastic T-cell lymphoma (AITL) or follicular helper T-cell lymphoma, angioimmunoblastic type), nodal T follicular helper cell lymphoma follicular type (also known as follicular helper T-cell lymphoma, follicular type), or nodal T follicular helper cell lymphoma NOS (also known as follicular helper T-cell lymphoma, NOS)), or other peripheral T-cell lymphomas (e.g., peripheral T-cell lymphoma NOS)))))).

26. The method of claim 25, wherein the hematological cancer is selected from the group consisting of lymphomas (e.g., non-Hodgkin lymphoma (e.g., B cell lymphoid proliferations and lymphomas (e.g., mature B cell neoplasms (e.g., large B cell lymphoma (e.g., diffuse large B-cell lymphoma not otherwise specified (DLBCL-NOS), or primary mediastinal large B cell lymphoma (primary mediastinal LBCL)), follicular lymphoma (FL), or transformations of indolent B cell lymphomas)), T-cell and NK-cell lymphoid proliferations and lymphomas (e.g., mature T-cell and NK-cell neoplasms (e.g., primary cutaneous T-cell lymphoid proliferations and lymphomas (cutaneous T-cell lymphoma (CTCL)) (e.g., primary cutaneous CD4-positive small or medium T-cell lymphoproliferative disorder, or mycosis fungoides, or Sezary syndrome), or peripheral T-cell lymphoma (PTCL) (e.g., nodal T follicular helper cell lymphoma (e.g., nodal T follicular helper cell lymphoma angioimmunoblastic type (also known as angioimmunoblastic T-cell lymphoma (AITL) or follicular helper T-cell lymphoma, angioimmunoblastic type), nodal T follicular helper cell lymphoma follicular type (also known as follicular helper T-cell lymphoma, follicular type), or nodal T follicular helper cell lymphoma NOS (also known as follicular helper T-celllymphoma, NOS)), or other peripheral T-cell lymphomas (e.g., peripheral T-cell lymphoma NOS)))))).

27. The method of claim 25, wherein the hematological cancer is FL.

28. The method of claim 25, wherein the hematological cancer is DLBCL.

29. The method of any one of claims 23-28, wherein the cancer is positive for BCL6 expression (e.g., as determined by an IHC test).

30. The method of any one of claims 23-29, wherein the therapeutically effective amount of a compound of any one of claims 1-21, or a pharmaceutically acceptable salt thereof, or a pharmaceutical composition according to claim 22, is administered to the subject as a monotherapy.

31. The method of any one of claims 23-29, comprising administering an additional therapy or therapeutic agent to the subject.

32. The method of claim 31, wherein the additional therapy or therapeutic agent is a PI3K inhibitor, an Abl inhibitor (e.g., a BCR-Abl inhibitor), a BTK inhibitor, a JAK inhibitor, a BRaf inhibitor, a MEK inhibitor, a BCL-2 inhibitor, a Bcl-XL inhibitor, an XPO1 inhibitor, an inhibitor of the polycomb repressive complex 2 (PRC2), an immunomodulatory imide drug, anti-CD19 therapy, anti-CD20 therapy, anti-CD3 therapy, chemotherapy, or a combination thereof.

33. The method of claim 32, wherein the additional therapy or therapeutic agent is an inhibitor of the PRC2 (e.g., an EZH1 / 2 or EZH2 inhibitor).

34. A method for treating or preventing an autoimmune condition in a subject in need thereof, the method comprising administering to the subject a therapeutically effective amount of a compound of any one of claims 1-21, or a pharmaceutically acceptable salt thereof, or a pharmaceutical composition according to claim 22.

35. A method for treating a lymphoproliferative disorder in a subject in need thereof, the method comprising administering to the subject a therapeutically effective amount of a compound of any one of claims 1-21, or a pharmaceutically acceptable salt thereof, or a pharmaceutical composition according to claim 22.

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