CYCLIC COMPOUNDS AND METHODS OF USE THEREOF.

Abstract

This application relates to compounds of Formula (I), as defined herein, and pharmaceutically acceptable salts thereof, which are MALT1 inhibitors. This application also describes a pharmaceutical composition comprising a compound of Formula (I), and pharmaceutically acceptable salts thereof, and methods for using the compounds and compositions to treat diseases, such as cancer, autoimmune disorders, and inflammatory disorders.

Description

CYCLIC COMPOUNDS AND METHODS OF USE OF THESE DESCRIPTION OF ELECTRONICALLY SUBMITTED TEXT FILE The contents of the text file submitted electronically herewith are incorporated herein by reference in their entirety: a machine-readable copy of the sequence listing with file name: 173670076wo1 .txt, date of registration December 24, 2020, file size «214 kilobytes. TECHNICAL FIELD The present application relates to tricyclic and other multicyclic compounds that are useful for treating proliferative disorders such as cancer, as well as autoimmune and inflammatory disorders. BACKGROUND MALT1 (mucosal-associated lymphoid tissue lymphoma translocation protein 1) is an intracellular protein involved in lymphocyte proliferation through upstream NF-κΒ signaling to control lymphocyte activation, survival, proliferation, and differentiation. Together with a CARMA or CARD scaffolding protein (for example, CARD11 (caspase recruitment domain family member 11, also known as CARMA1), CARD14 (caspase recruitment domain family member 14, also known as CARMA2), CARD10 (caspase recruitment domain family member 10, also known as CARMA3) or CARD9 (caspase recruitment domain family member 9)) and BCL10 (B cell CLL / lymphoma 10), MALT1 is one of the three subunits of the CBM complex that forms upon activation of the cell surface antigen receptor. See Jaworski et al., Cell Mol Life Science 2016, 73,459-473, and Juilland and Thome. Frontiers in Immunology 2018, 9,1927. MALT1 is known to mediate NF-κΒ signaling through at least two mechanisms: first, MALT1 functions as a scaffolding protein and recruits NF-κΒ signaling proteins such as TRAF6, TAB (e.g., TAB1, TAB2, TAB3), TAK1 and ΝΕΜΟ-ΙΚΚα / β; and secondly, as a cysteine ​​protease, it cleaves and inactivates negative regulators of NF-κΒ signaling, such as RelB, A20 or CYLD. See Rosebeck et al., Science, 2011, 331,468-472. The protease activity of MALT1 has emerged as a potential therapeutic target, particularly where NF-κΒ and related pathways are thought to play a significant role. Activated diffuse large B cell-like lymphomas (ABC-DLBCL) are aggressive lymphomas often characterized by hyperactivation of NFkB, and it has been shown that inhibition of the MALT1 protease can dramatically inhibit growth and promote apoptosis of highly aggressive ABC-type DLBCLs. See Ferch U, et al., J Exp Med 2009, 206, 2313-2320; see also Hailfinger S, et al., Proc Nati Acad Sel USA 2009, 106, 19946-19951. Known peptide substrates of MALT1, or the API2-MALT1 fusion protein, include A20, CYLD, BCL10, RelB, regnase-1, roquine-1, NIK, and LIMA. See Rebeaud etal., Nat Immunol 2008, 9, 272-281; see also Coornaert et al., Nat Immunol 20008, 9, 263-271; Staal et al., EMBOJ 2011,30,1742-1752; Hailfingeretal., PNAS2011,108,14596-14601; Jeltsch et / ., Nat Immunol 2014,15,1079 QAFQCn / ZZnZ / q / ΥΙΛΙ 1089; Uehata et al., Cell 2013,153,1036-1049; Nie et al., Nat Commun 2015, 6, 5908; and Baens et al., PLoS ONE 2014, 9, e103774. A general profile of MALT1 substrates is described in Kasperkiewicz, etal. Scientific Reports 8.1 (2018): 1-10. Furthermore, several chromosomal translocations have been identified that lead to the generation of constitutively active MALT1 in ABC-DLBCL and the identification of the MALT1 fusion protein API2-MALT1 / lgH-MALT1 that leads to the activation of NF-κΒ independently of the Upstream stimulation further highlights the importance of this protein in cancer and various diseases. See Farinha et al., J Clinical Oncology 2005,23, 63706378. Furthermore, MALT1 has been shown to be involved in several different types of cancer, for example, hematological malignancies such as mantle cell lymphoma, chronic lymphocytic leukemia ( CLL) and solid tumors such as lung adenocarcinoma, breast cancer, pancreatic cancer and glioblastoma. See Jiang et al., Cancer Research 2011,71,2183-2192; see also Pan et al., Mol Cancer Res 2016,14,93-102, Penas etal., Blood 2010,115, 2214-2219 and J Cell Mol Med., July 2020;24(13):7550-7562. MALT1, as an immunomodulatory protein, is also involved in innate and adaptive immunity and may have effects on various inflammatory disorders, for example, psoriasis, multiple sclerosis, rheumatoid arthritis, Sjógren's syndrome, ulcerative colitis and different types of allergic disorders resulting from Chronic inflamation. See Afofina et al., FEBS Journal 2015, DOI: 10.1 111 / febs. 13325; see also Lowes et al., Ann Review Immunology 2014, 32, 227-255; Jabara et al., J Allergy Clin Immunology 2013,132,151-158; Streubel et al., Clin Cancer Research 2004, 10, 476-480; and Liu et al., Oncotarget 2016, 1-14. Recent findings also suggest the importance of MALT1 in controlling regulatory T cell (Treg) function and homeostasis. Studies are ongoing to confirm the potential of MALT1 inhibitors for the treatment of patients with solid tumors alone or in combination with immune checkpoint mechanisms. However, there are currently no MALT1 inhibitors approved for therapeutic use. COMPENDIUM Accordingly, a compound of Formula (I) is provided herein: or a pharmaceutically acceptable salt thereof, wherein at the moment. Also provided herein is a pharmaceutical composition comprising a compound of Formula (I), or a pharmaceutically acceptable salt thereof, and at least one pharmaceutically acceptable excipient. Also provided are methods of treating a type of cancer associated with the CBM complex pathway in a subject in need thereof, comprising administering to the subject an effective amount of a compound of Formula (I), or a potentially acceptable salt. pharmaceutical view thereof, or a pharmaceutical composition as described herein. Also provided are methods for treating a type of cancer in a subject in need thereof, comprising: (a) identify the cancer type as a cancer type associated with the CBM complex pathway; and (b) administering to the subject an effective amount of a compound of Formula (I), or a pharmaceutically acceptable salt thereof, or a pharmaceutical composition as described herein. Also provided are methods of treating a cancer in a subject in need thereof, comprising: administering an effective amount of a compound of Formula (I), or a pharmaceutically acceptable salt thereof, or a pharmaceutical composition as set forth describes herein a subject in whom a cancer associated with the CBM complex pathway was identified. Also provided are methods of treating a MALT1-associated cancer in a subject, comprising administering to a subject identified or diagnosed with a MALT1-associated cancer an effective amount of a compound of Formula (I), or a potentially acceptable salt. pharmaceutical view thereof, or a pharmaceutical composition as described herein. Also provided are methods of treating cancer in a subject in need thereof, comprising: (a) determine that the cancer type is associated with a deregulation of a MALT1 gene, a MALT1 protease, or the expression, activity or level of any of these; and (b) administering to the subject an effective amount of a compound of Formula (I), or a pharmaceutically acceptable salt thereof, or a pharmaceutical composition as described herein. Also provided are methods of inhibiting metastasis in a subject having a type of cancer in need thereof, comprising administering to the subject an effective amount of a compound of Formula (I), or a pharmaceutically acceptable salt of this, or a pharmaceutical composition as described herein. Also provided are methods of treating an autoimmune disorder in a subject in need thereof, comprising administering to the subject an effective amount of a compound of Formula (I), or a pharmaceutically acceptable salt thereof, or a composition pharmaceutical as described herein. Also provided are methods of treating a disease or disorder associated with the CBM complex pathway in a subject in need thereof, comprising administering to the subject an effective amount of a compound of Formula (I), or a medically acceptable salt. from a pharmaceutical point of view thereof, or a pharmaceutical composition as described herein. Also provided are methods of treating a disease or disorder in a subject in need thereof, comprising: (a) identify the type of cancer as a disease or disorder associated with the CBM complex pathway; and (b) administering to the subject an effective amount of a compound of Formula (I), or a pharmaceutically acceptable salt thereof, or a pharmaceutical composition as described herein. Also provided are methods of treating a disease or disorder in a subject in need thereof, comprising: administer an effective amount of a compound of Formula (I), or a pharmaceutically acceptable salt thereof, or a pharmaceutical composition as described herein, to a subject who has been identified as having a disease or a disorder associated with the CBM complex pathway. Also provided are methods of treating a MALT1-associated autoimmune disorder in a subject, comprising administering to a subject identified or diagnosed with a MALT1-associated autoimmune disorder an effective amount of a compound of Formula (I), or an acceptable salt thereof. the pharmaceutical point of view thereof, or a pharmaceutical composition as described herein. Also provided are methods of treating a MALT1-associated autoimmune disorder in a subject, comprising administering to a subject identified or diagnosed with a MALT1-associated autoimmune disorder an effective amount of a compound of Formula (I), or an acceptable salt thereof. the pharmaceutical point of view thereof, or a pharmaceutical composition as described herein. Also provided are methods of treating an autoimmune disorder in a subject in need thereof, comprising: (a) determining that the autoimmune disorder is associated with a deregulation of a MALT1 gene, a MALT1 protease, or the expression, activity or level of any of these; and (b) administering to the subject an effective amount of a compound of Formula (I), or a pharmaceutically acceptable salt thereof, or a pharmaceutical composition as described herein. Also provided are methods of treating a MALT1-associated autoimmune disorder in a subject, comprising administering an effective amount of a compound of Formula (I), or a pharmaceutically acceptable salt thereof, or a pharmaceutical composition such as Described herein, a subject who was determined to have a MALT1-associated autoimmune disorder. Also provided are methods of treating an inflammatory disorder in a subject in need thereof, comprising administering to the subject an effective amount of a compound of Formula (I), or a pharmaceutically acceptable salt thereof, or a composition pharmaceutical as described herein. Also provided are methods of treating a MALT1-associated inflammatory disorder in a subject, comprising administering to a subject identified or diagnosed with a MALT1-associated inflammatory disorder an effective amount of a compound of Formula (I), or an acceptable salt thereof. pharmaceutical point of view thereof, or a pharmaceutical composition as described herein. Also provided are methods of treating a MALT1-associated inflammatory disorder in a subject, comprising administering to a subject identified or diagnosed with a MALT1-associated inflammatory disorder an effective amount of a compound of Formula (I), or an acceptable salt thereof. pharmaceutical point of view thereof, or a pharmaceutical composition as described herein. Also provided are methods of treating an inflammatory disorder in a subject in need thereof, comprising: (a) determining that the inflammatory disorder is associated with a deregulation of a MALT1 gene, a MALT1 protease, or the expression, activity or level of any of these; and QRFQCn / ZZnZ / q / ΥΙΛΙ (b) administer to the subject an effective amount of a compound of Formula (I), or a pharmaceutically acceptable salt thereof, or a pharmaceutical composition as described herein. Also provided are methods of treating a MALT1-associated inflammatory disorder in a subject, comprising administering an effective amount of a compound of Formula (I), or a pharmaceutically acceptable salt thereof, or a pharmaceutical composition such as Described herein, a subject who was determined to have a MALT1-associated inflammatory disorder. Also provided are methods for inhibiting the activity of the CBM complex pathway in a mammalian cell, comprising contacting the mammalian cell with a compound of Formula (I), or a pharmaceutically acceptable salt of this. Also provided are methods for inhibiting MALT1 protease activity in a mammalian cell, comprising contacting the mammalian cell with a compound of Formula (I), or a pharmaceutically acceptable salt thereof. Also provided is the use of compounds of Formula (I), or pharmaceutically acceptable salts thereof, to treat a disease or disorder associated with the CBM complex pathway. Also provided are compounds of Formula (I), or pharmaceutically acceptable salts thereof, for use in the preparation of a medicament for the treatment of a disease or disorder associated with the CBM complex pathway. Also provided are methods of treating an individual with a MALT1-associated cancer that include administering a compound of Formula (I), or a pharmaceutically acceptable salt thereof, before, during or after the administration of other antineoplastic drugs (for example, a first MALT1 inhibitor or another MALT1 inhibitor). Also provided herein is a process for preparing a compound of Formula (I), or a pharmaceutically acceptable salt thereof. Also provided herein is a compound of Formula (I), or a pharmaceutically acceptable salt thereof, obtained by a compound preparation process as defined herein. Unless otherwise defined, all technical and scientific terms used herein have the same meaning as commonly understood by a person of the mid-level trade to which this disclosure pertains. Methods and materials for use in the present disclosure are described herein; Other suitable methods and materials known in the art may also be used. The materials, methods and examples are illustrative only and are not intended to be limiting. All publications, patent applications, patents, sequences, database entries and other references mentioned herein are incorporated by reference in their entirety. In the event of a conflict, this specification, including definitions, shall prevail. Other features and advantages of the disclosure will be apparent from the following detailed description and claims. QRQQcn / zznz / q / υιλι DETAILED DESCRIPTION Definitions The term compound, as used herein, includes all stereoisomers, geometric isomers, tautomers and isotopically enriched variants of the structures represented. Compounds identified herein by name or structure as a particular tautomeric form are intended to include other tautomeric forms unless otherwise specified. As used herein, the term tautomer refers to compounds whose structures differ markedly in the arrangement of atoms, but which exist in easy and rapid equilibrium, and it should be understood that the compounds provided herein may be represented as different tautomers. , and, when the compounds have tautomeric forms, it is intended that all tautomeric forms are within the scope of the disclosure, and the naming of the compounds does not exclude any tautomers. The following is an example of tautomeric forms included: OH O Λ Á Λ Λ Ν _ 5 ΝΗ b .I b j It will be appreciated that certain compounds provided herein may contain one or more centers of asymmetry and, therefore, may be prepared and isolated in a mixture of isomers such as a racemic mixture, or in an enantiomerically pure form. The term halo refers to one of the halogens, group 17 of the periodic table. In particular, the term refers to fluorine, chlorine, bromine and iodine. Preferably, the term refers to fluorine or chlorine. The term C1-C6 alkyl refers to a straight or branched hydrocarbon chain containing 1,2, 3, 4, 5 or 6 carbon atoms, for example, methyl, ethyl, n-propyl, iso-propyl, n- butyl, sec-butyl, tert-butyl, n-pentyl and n-hexyl. Similarly, a C1-C3 alkyl group is a straight or branched hydrocarbon chain containing 1,2, or 3 carbon atoms. The term C1-C6 haloalkyl refers to a hydrocarbon chain substituted with at least one halogen atom chosen independently in each case, for example, fluorine, chlorine, bromine and iodine. The halogen atom can be present at any position in the hydrocarbon chain. Similarly, a C1-C3 haloalkyl group is a straight or branched hydrocarbon chain containing 1,2, or 3 carbon atoms substituted with at least one halogen atom. For example, C1-C3 haloalkyl may refer to chloromethyl, fluoromethyl, trifluoromethyl, chloroethyl, for example, 1-chloroethyl and 2-chloroethyl, trichloroethyl, for example, 1,2,2-trichloroethyl, 2,2,2-trichloroethyl, fluoroethyl, for example, 1-fluoromethyl and 2-fluoroethyl, trifluoroethyl, for example, 1,2,2-trifluoroethyl and 2,2,2-trifluoroethyl, chloropropyl, trichloropropyl, fluoropropyl, trifluoropropyl. The term C1-C6 alkoxy refers to a C1-C6 alkyl group that is attached to a molecule by oxygen. This includes moieties where the alkyl moiety may be linear or branched, such as methoxy, ethoxy, n-propoxy, iso-propoxy, QRQQcn / zznz / q / υιλι n-butoxy, sec-butoxy, tert-butoxy, n-pentox¡ and n-hexoxy¡. The term C1-C6 haloalkoxy refers to a C1-C6 alkyl group that is attached to a molecule by oxygen and where at least one hydrogen atom of the alkyl group is replaced with a halogen. This includes portions where the alkyl moiety may be linear or branched, such as fluoromethoxy, difluoromethoxy, trifluoromethoxy, 2,2,2trifluoroethoxy or trifluoropropoxy. represents a single or double bond, if the valence allows it. For example, As used herein, the term cyano refers to a -CN radical. As used herein, the term hydroxyl refers to an -OH radical. As used herein, the term amino refers to a -NH2 group. As used herein, the term aryl refers to a 6-10 membered, all carbon, mono or bicyclic group where at least one ring in the system is aromatic. Non-limiting examples of aryl groups include phenyl, naphthyl, tetrahydronaphthyl. In bicyclic ring systems where only one ring is aromatic, the non-aromatic ring may be a cycloalkyl group, as defined herein. As used herein, the term heteroaryl refers to a 5-10 membered mono- or bicyclic group where at least one ring of the system is aromatic; wherein one or more carbon atoms in at least one ring of the system are replaced by a heteroatom independently selected from N, O and S. Heteroaryl groups include rings in which one or more groups are oxidized, such as a pyridone moiety. Non-limiting examples of heteroaryl groups include pyridine, pyrimidine, pyrrole, imidazole and indole. In bicyclic ring systems in which only one ring is aromatic, the non-aromatic ring may be a cycloalkyl or heterocyclyl group, as defined herein. As used herein, the term cycloalkyl refers to a saturated or partially unsaturated 3-10 membered mono- or bicyclic hydrocarbon group; wherein bicyclic systems include fused, spiro (optionally referred to as spirocycloalkyl groups), and bridged ring systems. Non-limiting examples of cycloalkyl groups include cyclopropyl, cyclohexyl, spiro[2.3]hexyl and bicyclo[1.1.1]pentyl. The term heterocyclyl refers to a saturated or partially unsaturated 3-12 membered monocyclic or bicyclic hydrocarbon ring system, which is non-aromatic and has at least one heteroatom within the ring selected from N, O and S. Heterocyclyl groups Bicyclics include fused, spiro (optionally called spiroheterocyclyl groups), and bridged ring systems. The heterocyclyl ring system may include an oxo substitution on one or more C, N or S ring members. The heterocyclyl group may be denoted as, for example, a 5-10 membered heterocyclyl group, which is a ring system containing 5, 6, 7, 8, 9 or 10 atoms, where at least one is a heteroatom. For example, there may be 1, 2 or 3 heteroatoms, optionally 1 or 2. The heterocyclyl group may be attached to the rest of the molecule through any carbon atom or through a heteroatom such as nitrogen. Exemplary heterocyclyl groups include, but are not limited to, piperidinyl, piperazinyl, morpholino, tetrahydropyranyl, azetidinyl, oxetanyl, 2-azaspiro[3.3]heptanyl, pyrrolidin-2-one, sulfolane, S,S-isothiazoline dioxide and decahydronaphthalenyl. As used herein, the term geminal refers to atoms or substituent groups attached to the same atom in a molecule. As used herein, the term vicinal1' refers to atoms or substituent groups attached to adjacent atoms in a molecule. The stereochemical relationship between atoms or substituent groups can be cis, trans, undefined or unresolved. As used herein, the term oxo refers to a '-O group attached to a carbon atom. As used herein, the symbol represents the point of attachment of an atom or portion to the indicated atom or group in the rest of the molecule. It should be understood that the ring in the compounds of Formula (I) comprising atoms X, Y and Z does not contain more than two adjacent nitrogen atoms. The compounds of Formula (I) include pharmaceutically acceptable salts thereof. Furthermore, compounds of Formula (I) also include other salts of such compounds which are not necessarily pharmaceutically acceptable salts and which may be useful as intermediates for preparing and / or purifying compounds of Formula (I) and / or to separate enantlomers of compounds of Formula (I). Non-limiting examples of pharmaceutically acceptable salts of compounds of Formula (I) include trifluoroacetic acid and hydrochloride salts. It will be further appreciated that the compounds of Formula (I) or their salts can be isolated in the form of solvates and, therefore, any such solvate is included within the scope of the present disclosure. For example, the compounds of Formula (I) and salts thereof may exist in both unsolvated and solvated forms with pharmaceutically acceptable solvents such as water, ethanol and the like. In some embodiments, the compounds of Formula (I) include the compounds of Examples 1-211 and stereoisomers and pharmaceutically acceptable salts thereof. In some embodiments, the compounds of Formula (I) include the compounds of Examples 1-211 and pharmaceutically acceptable salts thereof. In some embodiments, the compounds of Examples 1-211 are in free base form. In some embodiments, the compounds of Examples 1-211 are in the form of pharmaceutically acceptable salts. The expression acceptable from a pharmaceutical point of view indicates that the compound, or salt or composition thereof, is chemically and / or toxicologically compatible with the other ingredients that comprise a formulation and / or the subject that is treated with it. Protecting groups can be a temporary substituent that protects a potentially reactive functional group from unwanted chemical transformations. The choice of the particular protective group employed is within the knowledge of a mid-level trade person. Several considerations can determine the choice of protecting group, including, but not limited to, the functional group being protected, other functionality present in the molecule, the reaction conditions at each step of the synthetic sequence, other protecting groups present in the molecule, the tolerance of the functional group to the conditions necessary to remove the protecting group, and the reaction conditions for the thermal decomposition of the compounds provided herein. The field of protective group chemistry has been reviewed (Greene, T. W. and Wuts, P. G. M. Protective Groups in Organic Synthesis, 2nd ed. Wiley: New York, 1991). A nitrogen protecting group can be any temporary substituent that protects an amine moiety from unwanted chemical transformations. Examples of moieties formed when such protecting groups are attached to an amine include, but are not limited to, allylamine, benzylamines (e.g., bezylamine, p-methoxybenzylamine, 2,4dimethoxybenzylamine and tritylamine), acetylamide, trichloroacetamide, trifluoroacetamide, pent-4-enamide , phthalimides, carbamates (for example, methyl carbamate, t-butyl carbamate, benzyl carbamate, allyl carbamates, 2,2,2-trichloroethyl carbamate and 9-fluorenylmethyl carbamate), mines and sulfonamides (e.g. example, benzenesulfonamide, p-toluenesulfonamide and p-nitrobenzenesulfonamide). An oxygen protecting group can be any temporary substituent that protects a hydroxyl moiety from unwanted chemical transformations. Examples of moieties formed when such protecting groups are attached to a hydroxyl include, but are not limited to, esters (e.g., acetyl, t-butylcarbonyl and benzoyl), benzyl (e.g., benzyl, p-methoxybenzyl and 2,4-dimethoxybenzyl and triphyl), carbonates (for example, methyl carbonate, allyl carbonate, 2,2,2-trichloroethyl carbonate and benzyl carbonate), ketals, acetals and ethers. The compounds provided herein may also contain unnatural ratios of atomic isotopes in one or more of the atoms constituting such compounds. That is, an atom, in particular when mentioned in relation to a compound according to Formula (I), comprises all isotopes and isotopic mixtures of that atom, whether of natural or synthetic origin, in natural abundance or in the form isotopically enriched. For example, when hydrogen is mentioned, it is understood that it refers to 1H, 2H, 3H or mixtures of these; When carbon is mentioned, it is understood to refer to 11C, 12C, 13C, 14C or mixtures of these; When nitrogen is mentioned, it is understood that it refers to 13N,14N,15N or mixtures of these; When oxygen is mentioned, it is understood that it refers to 140,150,160,17O,18O or mixtures of these; and when fluoro is mentioned, it is understood that it refers to 18F, 19F or mixtures of these; unless expressly stated otherwise. For example, in deuteroalkyl and deuteroalkoxy groups, where one or more hydrogen atoms are specifically replaced with deuterium (2H). As some of the above-mentioned isotopes are radioactive, the compounds provided herein accordingly also comprise compounds with one or more isotopes of one or more atoms, and mixtures thereof, including radioactive compounds, wherein one or more non-radioactive atoms have been replaced by one of its radioactive enriched isotopes. Radiolabeled compounds are useful as therapeutic agents, for example, anticancer therapeutic agents, research reagents, for example, assay reagents, and diagnostic agents, for example, in vivo imaging agents. All isotopic variations of the compounds provided herein, whether radioactive or not, are intended to be included within the scope of the present disclosure. For illustrative purposes, general methods for preparing the compounds, as well as key intermediates, are provided herein. For a more detailed description of the individual reaction steps, see the Examples section below. Those of mid-level craft will appreciate that other synthetic routes can be used to synthesize the inventive compounds. While specific reagents and starting materials are illustrated in the Schemes and discussed below, they can be easily substituted with other reagents and starting materials to provide a variety of derivatives and / or reaction conditions. Furthermore, many of the compounds prepared with the methods described below can be further modified in light of this disclosure by conventional chemistry known to those of ordinary skill in the art. The ability of the selected compounds to act as MALT1 inhibitors can be demonstrated by the biological assays described herein. IC50 values ​​are shown in Table A. The compounds of Formula (I), or a pharmaceutically acceptable salt thereof, are useful for treating diseases and disorders that can be treated with a MALT1 inhibitor, such as MALT1-associated cancers, including types of hematological cancers and solid tumors, MALT1-associated autoimmune disorders and MALT1-associated inflammatory disorders. As used herein, the term treat or treatment refers to therapeutic or palliative measures. Beneficial or desired clinical outcomes include, but are not limited to, complete or partial relief of symptoms associated with a disease, disorder or condition, decreased extent of the disease, stabilized (i.e., no worsening) state of the disease, delay or slowing of disease progression, improvement or palliation of the pathological state (for example, one or more symptoms of the disease) and remission (whether partial or total), whether detectable or undetectable. Treatment may also mean prolonging survival compared to the expected survival without treatment. As used herein, the term subject refers to any animal, including mammals such as humans. In some embodiments, the subject is a human being. In some embodiments, the subject has experienced and / or exhibited at least one symptom of the disease or disorder to be treated and / or prevented. As used herein, the term pediatric subject refers to a subject under 21 years of age at the time of diagnosis or treatment. The term pediatric can be further divided into various subpopulations, including: newborns (from birth to the first month of life); babies (from 1 month to two years); children (from two years to 12 years); and adolescents (from 12 years to 21 years (up to and including the twenty-second birthday)). Berhman RE, Kliegman R, Arvin AM, Nelson WE. Nelson Textbook of Pediatrics, 15.aed. Philadelphia: W.B. Saunders Company, 1996; Rudolph AM, et al. Rudolph's Pediatrics, 21.aed. New York: McGraw-Hill, 2002; and Avery MD, First LR. Pediatrics Medicine, 2.aed. Baltimore: Williams & Wilkins; 1994. In some embodiments, a pediatric subject is from birth to the first 28 days of life, from 29 days to less than two years, from two years to less than 12 years, or from 12 years to 21 years. years (until the twenty-second birthday, not QRFQCn / ZZnZ / q / ΥΙΛΙ inclusive). In some embodiments, a pediatric subject is from birth to the first 28 days of life, from 29 days to less than 1 year, from one month to less than four months, from three months to less than seven months, from six months to less than 1 year, from 1 year to less than 2 years, from 2 years to less than 3 years, from 2 years to less than 7 years, from 3 years to less than 5 years, from from 5 years to less than 10 years, from 6 years to less than 13 years, from 10 years to less than 15 years or from 15 years to less than 22 years. In certain embodiments, the compounds of Formula (I), or a pharmaceutically acceptable salt thereof, are useful for preventing diseases and disorders defined herein (for example, autoimmune disorders, inflammatory disorders and cancer ). As used herein, the term prevent means the prevention of the onset, recurrence or spread, in whole or in part, of the disease or condition described herein, or a symptom thereof. The expression regulatory body refers to the entity in a country that is responsible for approving the medical use of pharmaceutical agents with the country. For example, a non-limiting example of a regulatory entity is the United States Food and Drug Administration (FDA). Signaling through the NF-κΒ pathway has been implicated in many types of cancer. See, for example, Staudt, Coid Spring Harbor Perspectives in Biology 2.6 (2010): a000109, Xia, et al. Cancer Immunol. Res. 2.9 (2014): 823-830, Xia, et al. OncoTargets and Therapy 11 (2018): 2063. NF-κΒ is a family of transcription factors, including p50, p52, p65 (RelA), RelB, and c-Rel, that can bind to the kB enhancer element as various homo- and heterodimers to induce the transcription of several genes. After activation of certain cell surface receptors (for example, CD28, BCR, HER1 (also known as EGFR (epidermal growth factor receptor) and ERBB1) or HER2 (also known as HER2 / neu or ERBB2)), A CBM complex is formed by phosphorylation of a CARD or CARMA protein, probably by a protein kinase C (e.g., protein kinase C beta or protein kinase C theta) and recruitment of the BCL10-MALT1 complex. See, for example, Xia, et al. OncoTargets and Therapy 11 (2018): 2063, Shi and Sun. Mol. Immunol. 68.2 (2015): 546-557, Xia, et al. Cancer Immunol. Res. 2.9 (2014): 823-830, and Pan, Mol. Cancer Res. 14.1 (2016):93-102. As noted above, the CBM complex may function as a scaffold protein in the activation of the NF-κΒ pathway. When formed, the CBM complex can activate the IKK complex (e.g., IKKy (also called NEMO), IKKa, and ΙΚΚβ), probably through ubiquitination (e.g., K63-linked ubiquitination) of MALT1, resulting in the recruitment, ubiquitination (e.g., K63-linked ubiquitination) and degradation of IKKy, which releases IKKa and ΙΚΚβ to phosphorylate IkB, resulting in ubiquitination (e.g., K48-linked ubiquitination) and degradation of IkB, which releases NF-κΒ transcription factors (usually of the NF-κB1 subtype: p50RelA and p50-cRel) to the nucleus. This cascade is likely mediated by the ubiquitin ligase TRAF6 (tumor necrosis factor receptor (TNFR)-associated factor 6). The CBM complex can also affect NF-κΒ signaling through additional protein complexes, such as ΤΑΒ1 / 2-ΤΑΚ and linear ubiquitin chain assembly complex (LUBAC). See, for example, Israel, Coid Spring Harbor Perspectives in Biology 2.3 (2010): a000158, Xia, QRQQcn / zznz / q / υιλι etal. OncoTargets and Therapy 11 (2018): 2063, Juilland, Front. Immunol. 9 (2018): 1927. MALT1 can also activate the JNK pathway (also called the JNK / AP-1 pathway), although less work has been done to study this area. See, for example, Juilland, Front. Immunol. 9 (2018): 1927, and Wang, etal., Oncogenesis 6.7 (2017): e365-e365. Additionally, MALT1 has cysteine ​​protease activity. Non-limiting examples of wild-type MALT1 substrates include BCL10, A20, CYLD, RelB, regnase-1, roquina-1, and HOIL1. Furthermore, the API2-MALT1 fusion protein (also called clAP2; amino-terminal inhibitor of apoptosis 2) has also been shown to cleave NIK and LIMAIa. Cleavage of BCL10 by MALT1 is thought to result in BCL10-independent activation of NF-κΒ. By cleaving A20 (TNF alpha-induced protein 3), MALT1 may reduce the negative regulation of the NF-κΒ pathway, as A20 is a deubiquitinating enzyme that has been suggested to reduce MALT1 ubiquitination and therefore recruitment and the activation of the IKK complex. CYLD (CYLD Usine 63 deubiquitinase) is a deubiquitinating enzyme and, by cleaving this enzyme, MALT1 is thought to increase signaling through the NF-κΒ pathway and / or JNK pathway. Cleavage of RelB normally results in relief of negative regulation of the NF-κΒ pathway, as RelB forms transcriptionally inactive complexes with RelA and c-Rel. By cleaving HOIL1 (also known as RBCK1), downregulation of NF-κΒ is thought to be alleviated, as HOIL1 is thought to reduce linear ubiquitination. MALT1 can also be self-processed, promoting signaling through the NF-κΒ pathway through a mechanism that is not fully understood. By cleaving NIK (NF-κΒ-inducing kinase), the API2-MALT1 protease generates a C-terminal fragment of NIK that is resistant to proteasomal degradation and thus increases non-canonical NF-κΒ signaling. By cleaving LIMA1a (LIM domain and actin binding protein 1), the tumor suppressor properties of this protein are decreased, and the remaining fragment is believed to have oncogenic properties and enhance cell proliferation, colony formation, and cell adhesion. . Cleavage of regnase-1 (regulatory RNase 1, also known as MCPIP-1 or Zc3h12a) and rokine-1 (also known as RC3H1) is thought to result in the stabilization of mRNAs, including those for cytokines, chemokines and costimulatory proteins such as ICOS, OX40 and TNF. This activity may be independent of MALT1 activity in the NF-κΒ and JNK pathways. See, for example, Afonina, et al. FEBS J. 282.17 (2015): 3286-3297 Klein etal. Nat. Comm. 6.1 (2015): 1-17, Baens, etal. PloS one 9.8 (2014): e103774, and Juilland, Front. Immunol. 9 (2018): 1927. MALT1 also participates in oncogenic BCR signaling in cell lines and biopsy samples that respond to ibrutinib, coordinated by a multiprotein supercomplex consisting of MYD88, TLR9 and BCR (hereinafter referred to as My-T-supercomplex). BCR). The My-T-BCR supercomplex colocalizes with mTOR in endolysosomes, where it drives pro-survival NF-κΒ and mTOR signaling. See Phelan et al., Nature 2018 Aug;560(7718):387-391. Consequently, inhibition of MALT 1 may provide beneficial effects for many types of disorders associated with abnormal signaling in the NF-κΒ pathway or JNK pathway. For example, inhibition of MALT 1 may decrease flux through the NF-κΒ or JNK pathways resulting in one or more of: (1) An inactivated tumor suppressor gene. Non-limiting examples of tumor suppressor genes that can be inactivated include BRCA1 and p53 (e.g., p53 H61L or I123T). See, for example, Sau, et al. Cell Stem Cell 19.1 (2016): 52-65, Xia, etal. Cancer Immunol. Res. 2.9 (2014): 823-830, Johansson, etal. Oncotarget7.38 (2016): 62627. QRFQCn / ZZnZ / q / ΥΙΛΙ (2) A dysregulated cell surface receptor. Non-limiting examples of cell surface receptors include HER1 and HER2. See, for example, Xia, et al. Cancer Immunol. Res. 2.9 (2014): 823-830 and Pan, Mol. Cancer Res. 14.1 (2016): 93-102. (3) Deregulation of one or more components of a CBM complex. Non-limiting examples of components of a CBM complex include MALT1, CARD11, CARD14, CARD10, CARD9, and BCL10. (4) Deregulation of one or more substrates of a MALT1 protease (e.g., a wild-type MALT1 protease or a deregulated MALT1 protease). Non-limiting examples of substrates of a MALT1 protease include BCL10, A20, CYLD, RelB, regnase-1, roquine-1, HOIL1, NIK, and LIMAIa. (5) Deregulation of one or more components of the NF-κΒ pathway downstream of a CBM complex. Non-limiting examples of a component of the NF-κΒ pathway downstream of a CBM complex include TRAF6, ΙΚΚα, ΙΚΚβ, ΙΚΚγ (also called NEMO), IkBa, p50, p52, p65 (RelA), RelB and c-Rel. (6) Deregulation of one or more components of the JNK pathway downstream of a CBM complex. Non-limiting examples of a JNK pathway component downstream of a CBM complex include JNK1 (mitogen-activated protein kinase 8), JNK2 (mitogen-activated protein kinase 9), JNK3 (mitogen-activated protein kinase 10), or a factor of AP-1 transcription (for example, a heterodimer from any of the c-Fos, c-Jun, ATF or JDP families). (7) Deregulation of one or more fusion proteins caused by chromosomal translocation of the MALT1 gene. Non-limiting example includes the CIAP-MALT1 fusion protein. (8) Deregulation of one or more components of the My-T-BCR supercomplex. Non-limiting examples of a component of the My-T-BCR supercomplex include MYD88, TLR9 and mTOR. The expression pathway of the CBM complex as associated herein includes genes, transcripts and proteins in a signal transduction pathway that includes a CBM. For example, many aspects of the NF-κΒ pathway are part of a CBM complex pathway. A CBM complex pathway may include, for example, cell surface receptors (e.g., CD28, BCR, HER1 and HER2), a signal transducer between a cell surface receptor and a CBM complex (e.g., a protein kinase C beta or protein kinase C theta), a component of a CBM complex (e.g., MALT1, CARD11, CARD14, CARD10, CARD9 or BCL10), substrates of a MALT1 protease (e.g., BCL10, A20, CYLD, RelB, regnase-1, roquine-1, HOIL1, NIKy LIMAIa), a component of the NF-κΒ pathway downstream of a CBM complex (e.g., TAK1, TRAF6, TAB1, TAB2, TAB3, MKK7, ΙΚΚα, ΙΚΚβ, ΙΚΚγ, IkBa, p50, p65 (RelA), or c-Rel), a component of the JNK pathway downstream of a CBM complex (e.g., JNK1, JNK2, JNK3, or an AP-1 transcription factor), or a component of the My supercomplex -T-BCR (for example, MYD88, TLR9 or mTOR). As used herein, the term CBM complex pathway-associated disease or disorder refers to diseases or disorders associated with or having a deregulation of a gene in a CBM complex pathway, a protein in a CBM complex pathway , or the expression, activity or level of any (e.g., one or more) of these (e.g., any type of deregulation of a gene in a CBM complex pathway, a protein in a CBM complex pathway, or the expression, activity or level of any of these, as described herein). Non-limiting examples of diseases or disorders associated with the CBM complex pathway include, for example, CBM-related primary immunodeficiency diseases, autoimmune disorders, multiple sclerosis, colitis, psoriasis and cancer. See, for example, McGuire, et al. J. Neuroinflamm. 11.1 (2014): 1-12, Lu, etal., Front. Immunol. 9 (2018): 2078, Jaworski, et al., EMBOJ. 33.23 (2014): 2765-2781. Non-limiting examples of a disease or disorder associated with the CBM complex pathway include MALT1-associated diseases or disorders such as MALT1-associated cancers, MALT1-associated autoimmune disorders, and MALT1-associated inflammatory disorders. As used herein, the term CBM complex pathway-associated autoimmune disorder refers to autoimmune disorders associated with or having a deregulation of a CBM complex pathway gene, a CBM complex pathway protein, or the expression, activity or level of any (for example, one or more) of these (for example, any type of deregulation of a CBM complex pathway gene, a CBM complex pathway protein, or the expression , activity or level of any of these described herein). Non-limiting examples of autoimmune disorders associated with the CBM complex pathway are described herein. As used herein, the term CBM complex pathway-associated inflammatory disorder refers to inflammatory disorders associated with or having a deregulation of a CBM complex pathway gene, a CBM complex pathway protein, or the expression, activity or level of any (for example, one or more) of these (for example, any type of deregulation of a CBM complex pathway gene, a CBM complex pathway protein, or the expression , activity or level of any of these described herein). Non-limiting examples of inflammatory disorders associated with the CBM complex pathway are described herein. In some embodiments, a disease or disorder associated with the CBM complex pathway is a type of cancer associated with the CBM complex pathway, such as a type of cancer associated with the cell surface receptor of the CBM complex pathway. (for example, a type of cancer associated with CD28, a type of cancer associated with BCR, a type of cancer associated with HER1 or a type of cancer associated with HER2), a type of cancer associated with a signal transducer between a receptor of the cell surface and a CBM complex (for example, a protein kinase C beta (PKCP)-associated cancer or a protein kinase C theta (PCKO)-associated cancer), a component of a cancer type associated with the CBM complex (for example, a type of cancer associated with MALT 1, a type of cancer associated with CARD11, a type of cancer associated with CARD14, a type of cancer associated with CARD10, a type of cancer associated with CARD9 or a type of cancer associated with BCL10), a type of cancer associated with the MALT 1 protease substrate (for example, a type of cancer associated with BCL10, a type of cancer associated with A20, a type of cancer associated with CYLD, a type of RelB-associated cancer, a regnase-1-associated cancer, a roquine-1-associated cancer, a HOIL1-associated cancer, a NIK-associated cancer, or a LIMAIa-associated cancer), a type of cancer associated with a component of the NF-κΒ pathway downstream of a CBM complex (e.g., a type of cancer associated with TAK1, a type of cancer associated with TRAF6, a type of cancer associated with TAB1, a type of cancer associated with TAB2, a type of cancer associated with TAB3, a type of cancer associated with MKK7, a type of cancer associated with IKKa, a type of cancer associated with IΚΚβ, a type of cancer associated with IKKy, a type of cancer IkBa-associated, a p50-associated cancer, a p65 (RelA)-associated cancer, or a c-Rel-associated cancer), a cancer associated with a component of the JNK pathway downstream of a CBM complex (for example, a type of cancer associated with JNK1, a type of cancer associated with JNK2, a type of cancer associated with JNK3 or a type of cancer associated with the transcription factor AP-1), a type of cancer associated with MYD88 or a combination of these. As used herein, the term CBM complex pathway-associated cancer refers to types of cancer associated with or having a deregulation of a gene in a CBM complex pathway, a protein in a CBM complex pathway, or in the expression, activity or level of any (e.g., one or more) of these (e.g., any type of deregulation of a gene in a CBM complex pathway, a protein in a CBM complex pathway, or in the expression, activity or level of any of these, as described herein) (for example, after diagnosis or after developing resistance to previous treatments). Non-limiting examples of a type of cancer associated with the CBM complex pathway are described herein. In some embodiments, a type of cancer associated with the CBM pathway may be a type of cancer associated with the cell surface receptor of the CBM complex pathway (for example, a type of cancer associated with CD28, a type of BCR-associated cancer, a type of cancer associated with HER1 or a type of cancer associated with HER2), a type of cancer associated with a signal transducer between a cell surface receptor and a CBM complex (for example, a type of protein kinase C beta (PKCP)-associated cancer or a protein kinase C theta (PCK0)-associated cancer, a component of a CBM complex-associated cancer (e.g., a MALT 1-associated cancer) , a type of cancer associated with CARD11, a type of cancer associated with CARD14, a type of cancer associated with CARD10, a type of cancer associated with CARD9 or a type of cancer associated with BCL10), a type of cancer associated with the substrate MALT1 protease (for example, a type of cancer associated with BCL10, a type of cancer associated with A20, a type of cancer associated with CYLD, a type of cancer associated with RelB, a type of cancer associated with regnase-1, a type rokine-1-associated cancer, a HOIL1-associated cancer, a NIK-associated cancer, or a LIMA1-associated cancer, a) a cancer type associated with a downstream component of the NF-kB pathway of a CBM complex (for example, a type of cancer associated with TAK1, a type of cancer associated with TRAF6, a type of cancer associated with TAB1, a type of cancer associated with TAB2, a type of cancer associated with TAB3, a type of cancer associated with MKK7, a type of cancer associated with IKKa, a type of cancer associated with ΙΚΚβ, a type of cancer associated with IKKy, a type of cancer associated with IkBa, a type of cancer associated with p50, a type of cancer p65 (RelA)-associated cancer or a c-Rel-associated cancer), a cancer type associated with a component of the JNK pathway downstream of a CBM complex (e.g., a JNK1-associated cancer, a JNK2-associated cancer, a JNK3-associated cancer, or an AP-1 transcription factor-associated cancer) or a combination of these. In some embodiments, a dysregulation may be a dysregulation that results in abnormal activation of a gene, protein, or the expression, activity or level of any of these. Activation may be through any suitable mechanism, including, but not limited to, gene amplification, activating mutation, activating translocation, transcriptional activation, epigenetic alteration and / or overexpression of the oncogene protein product. In some embodiments, a deregulation may be a deregulation that results in abnormal inactivation of a gene, a protein, or the expression, activity or level of any of these. Inactivation may be through any suitable mechanism, including, but not limited to, gene deletion, inactivating mutation, QRQQcn / zznz / q / υιλι inactivating translocation, transcriptional silencing, epigenetic alteration and degradation of mRNA and / or protein products of the gene. Typically, as used herein, a deregulation, whether activation or inactivation, is a deregulation that results in increased signaling through the NFκB or JNK signal transduction pathways. The term "wild type" describes a nucleic acid (e.g., a MALT1 gene or a MALT1 mRNA) or protein (e.g., a MALT1 protein) that is found in a subject who does not have a disease or disorder associated with the nucleic acid. or protein (for example, the MALT1 gene, MALT1 mRNA, or MALT1 protein) (and, optionally, is also not at increased risk of developing a disease or disorder associated with the nucleic acid or protein and / or is not believed to have a disease or disorder associated with the gene or protein), or is found in a cell or tissue of a subject who does not have a disease or disorder associated with the gene or protein (for example, a type of cancer, autoimmune disorder or inflammatory disorder associated with MALT1) (and optionally also not at increased risk of developing a disease or disorder associated with the nucleic acid or protein and / or are not believed to have a disease or disorder associated with nucleic acid or protein. In some embodiments, the subject has been identified or diagnosed as having a type of cancer with a deregulation of a gene associated with the CBM complex pathway (e.g., a MALT1 gene), a protein associated with the CBM complex pathway. (for example, a MALT1 protein), or in the expression, activity or level of any of these (a type of cancer associated with the CBM complex pathway) (for example, as determined with an assay or kit approved by an entity regulator, for example, approved by the FDA). In some embodiments, the subject has a cancer resistant to one or more prior treatments. In some embodiments, the subject has a tumor positive for a deregulation of a gene associated with the CBM complex pathway (e.g., a MALT1 gene), a protein associated with the CBM complex pathway (e.g., a MALT1 protein ), or in the expression, activity or level of any of these (for example, as determined with an assay or kit approved by a regulatory body, for example, approved by the FDA). The subject may be a subject with a tumor or tumors positive for a deregulation of a gene associated with the CBM complex pathway (e.g., a MALT1 gene), a protein associated with the CBM complex pathway (a MALT1 protein), or the expression, activity or level of any of these (for example, identified as positive with an assay or kit approved by a regulatory body, for example, approved by the FDA). The subject may be a subject whose tumors have a deregulation of a gene associated with the CBM complex pathway (e.g., a MALT1 gene), a protein associated with the CBM complex pathway (e.g., a MALT1 protein), or in the expression, activity or level thereof (for example, where the tumor is identified as such with an assay or kit approved by a regulatory body, for example, approved by the FDA). In some embodiments, the subject has a tumor resistant to one or more prior treatments. In some embodiments, the subject is believed to have a cancer associated with the CBM complex pathway. In some embodiments, the subject has a tumor that is suspected to be resistant to one or more prior treatments. In some embodiments, the subject has a medical history indicating that the subject has a tumor that has a deregulation of a gene associated with the CBM complex pathway (e.g., a MALT1 gene), a protein associated with the CBM complex pathway. CBM complex (for example, a MALT1 protein), or in the expression, activity or level of any of these (and the clinical history QRQQcn / zznz / q / υιλι optionally indicates that the subject should be treated with any of the compositions provided herein). In some embodiments, the subject is a pediatric subject. In some embodiments, the subject has a clinical history indicating that the subject has a tumor resistant to one or more prior treatments. In some embodiments, the subject has been identified or diagnosed as having a type of cancer that, based on histological examination, is determined to be associated with a deregulation of a gene associated with the CBM complex pathway (e.g., a gene MALT1), a protein associated with the CBM complex pathway (for example, a MALT1 protein), or in the expression, activity or level of any of these (a type of cancer associated with the CBM complex pathway). In some embodiments, the subject has been identified or diagnosed as having an autoimmune disorder with a dysregulation of a gene associated with the CBM complex pathway (e.g., a MALT1 gene), a protein associated with the CBM complex pathway ( a MALT1 protein), or the expression, activity or level of any of these (an autoimmune disorder associated with the CBM complex pathway) (e.g., as determined with an assay or kit approved by a regulatory body, e.g., approved by the EDA). In some embodiments, the subject has a tumor positive for a deregulation of a gene associated with the CBM complex pathway (e.g., a MALT1 gene), a protein associated with the CBM complex pathway (a MALT1 protein), or the expression, activity or level of any of these (for example, as determined with an assay or kit approved by a regulatory body, for example, approved by the FDA). In some embodiments, the subject is believed to have an autoimmune disorder associated with the CBM complex pathway. In some embodiments, the subject has a medical history indicating that the subject has a tumor that has a deregulation of a gene associated with the CBM complex pathway (e.g., a MALT1 gene), a protein associated with the CBM complex pathway. CBM complex (a MALT1 protein), or the expression, activity or level of any of these (and the clinical history optionally indicates that the subject should be treated with any of the compositions provided herein). In some embodiments, the subject is a pediatric subject. In some embodiments, the subject has been identified or diagnosed as having an autoimmune disorder that, based on histological examination, is determined to be associated with a deregulation of a gene associated with the CBM complex pathway (e.g., a MALT1 gene ), a protein associated with the CBM complex pathway (a MALT1 protein), or the expression, activity or level of any of these (an autoimmune disorder associated with the CBM complex pathway). In some embodiments, the subject has been identified or diagnosed as having an inflammatory disorder with a dysregulation of a gene associated with the CBM complex pathway (e.g., a MALT1 gene), a protein associated with the CBM complex pathway ( a MALT1 protein), or the expression, activity or level of any of these (an inflammatory disorder associated with the CBM complex pathway) (e.g., as determined with an assay or kit approved by a regulatory body, e.g., approved by the FDA). In some embodiments, the subject has a tumor positive for a deregulation of a gene associated with the CBM complex pathway (e.g., a MALT1 gene), a protein associated with the CBM complex pathway (a MALT1 protein), or the expression, activity or level of any of these (for example, as determined with an assay or kit approved by a regulatory body, for example, approved by the FDA). In some embodiments, the subject is believed to have an inflammatory disorder associated with the CBM complex pathway. In some embodiments, the subject has a medical history indicating that the subject has a tumor that has a QRQQcn / zznz / q / υιλι deregulation of a gene associated with the CBM complex pathway (for example, a MALT1 gene), a protein associated with the CBM complex pathway (a MALT1 protein), or the expression, activity or level of any of these (and the clinical history optionally indicates that the subject should be treated with any of the compositions provided herein). In some embodiments, the subject is a pediatric subject. In some embodiments, the subject has been identified or diagnosed as having an inflammatory disorder that, based on histological examination, is determined to be associated with a deregulation of a gene associated with the CBM complex pathway (e.g., a MALT1 gene ), a protein associated with the CBM complex pathway (a MALT1 protein), or the expression, activity or level of any of these (an inflammatory disorder associated with the CBM complex pathway). As used herein, the term cancer associated with the cell surface receptor of the CBM complex pathway refers to types of cancer associated with or having a deregulation of a gene, a protein, or the expression, activity or level of any (e.g., one or more) of these associated with a cell surface receptor of the CBM complex pathway. In some embodiments, a type of cancer associated with the cell surface receptor of the CBM complex pathway is selected from the group consisting of a type of cancer associated with CD28, a type of cancer associated with BCR, a type of cancer HER1-associated, a type of HER2-associated cancer, and combinations of these. As used herein, the term *-associated cancer refers to types of cancer associated with or having a deregulation of a gene *, a protein *, or in the expression, activity or level of either (e.g., one or more) of these (for example, any of the types of deregulation of a gene *, a protein *, or in the expression, activity or level of any of these described herein), where it refers to a gene or a particular CBM complex pathway protein described herein. In some embodiments, the type of cancer associated with * is selected from the group consisting of: CD28 associated cancer, BCR associated cancer, HER1 associated cancer, HER2 associated cancer, ΡΚΟβ associated cancer, PKC8 associated cancer , MALT1-associated cancer, CARD11-associated cancer, CARD14-associated cancer, A20-associated cancer, CYLD-associated cancer, RelB-associated cancer, HOIL1-associated cancer, NIK-associated cancer, regnase-1-associated cancer, associated cancer a LIMA1 a, roquine-1 associated cancer, TRAF6 associated cancer, TAK1 associated cancer, TAB1 associated cancer, TAB2 associated cancer, TAB3 associated cancer, MKK7 associated cancer, IKKa associated cancer, ΙΚΚβ associated cancer , IKKy-associated cancer, IkBa-associated cancer, p50-associated cancer, p65-associated cancer, c-Rel-associated cancer, JNK1-associated cancer, JNK2-associated cancer, JNK3-associated cancer, MYD88 transcription factor-associated cancer and a cancer associated with the AP-1 transcription factor. In some embodiments, the *-associated cancer type is a CD28-associated cancer type. In some embodiments, the *-associated cancer type is a BCR-associated cancer type. In some embodiments, the *-associated cancer type is a HER1-associated cancer type. In some embodiments, the *-associated cancer type is a HER2-associated cancer type. In some embodiments, the *-associated cancer type is a ΡΚΟβ-associated cancer type. In some embodiments, the *-associated cancer type is a PKC8-associated cancer type. In some embodiments, the *-associated cancer type is a MALT1-associated cancer type. In some embodiments, the *-associated cancer type is a CARD11-associated cancer type. In some embodiments, the type of cancer associated with * is a type of cancer associated with QRQQcn / zznz / q / υιλι CARD14. In some embodiments, the cancer type associated with * is a cancer type associated with A20. In some embodiments, the *-associated cancer type is a CYLD-associated cancer type. In some embodiments, the *-associated cancer type is a RelB-associated cancer type. In some embodiments, the *-associated cancer type is a HOIL1-associated cancer type. In some embodiments, the *-associated cancer type is a NIK-associated cancer type. In some embodiments, the *-associated cancer type is a regnase-1-associated cancer type. In some embodiments, the *-associated cancer type is a LIMAIa-associated cancer type. In some embodiments, the type of cancer associated with * is a type of cancer associated with roquine-1. In some embodiments, the *-associated cancer type is a TRAF6-associated cancer type. In some embodiments, the *-associated cancer type is a TAK1-associated cancer type. In some embodiments, the *-associated cancer type is a TAB1-associated cancer type. In some embodiments, the *-associated cancer type is a TAB2-associated cancer type. In some embodiments, the *-associated cancer type is a TAB3-associated cancer type. In some embodiments, the *-associated cancer type is an MKK7-associated cancer type and an IKKa-associated cancer type. In some embodiments, the *-associated cancer type is a ΙΚΚβ-associated cancer type. In some embodiments, the *-associated cancer type is an IKKy-associated cancer type. In some embodiments, the *-associated cancer type is an IkBa-associated cancer type. In some embodiments, the *-associated cancer type is a p50-associated cancer type. In some embodiments, the *-associated cancer type is a p65-associated cancer type. In some embodiments, the *-associated cancer type is a c-Rel-associated cancer type. In some embodiments, the *-associated cancer type is a JNK1-associated cancer type. In some embodiments, the *-associated cancer type is a JNK2-associated cancer type. In some embodiments, the *-associated cancer type is a JNK3-associated cancer type. In some embodiments, the type of cancer associated with * is a type of cancer associated with the transcription factor AP-1. In some embodiments, the type of cancer associated with * is a type of cancer associated with the transcription factor MYD88. The phrase deregulation of a gene *, a protein *, or in the expression, activity or level of any of these (where * is a gene or a protein of the particular CBM complex pathway described herein) refers to a genetic mutation (for example, a chromosomal translocation that results in the expression of a fusion protein that includes a domain * and a fusion component, a mutation in a gene * that results in the expression of a protein * that includes a deletion of at least one amino acid compared to a wild-type * protein, a mutation in a gene * that results in the expression of a * protein with one or more point mutations compared to a wild-type * protein, a mutation in a gene * resulting in the expression of a protein * with at least one amino acid inserted compared to a wild-type protein *, a gene duplication resulting in a higher level of protein * in a cell, or a mutation in a regulatory sequence (e.g., a promoter and / or enhancer) that results in a higher level of protein * in a cell), an alternatively spliced ​​version of a * mRNA that results in a protein * that has a deletion of at least one amino acid in the protein * compared to the wild-type protein * or higher expression (e.g., higher QRFQCn / ZZnZ / q / ΥΙΛΙ levels) of a wild-type * protein in a mammalian cell due to abnormal cell signaling and / or dysregulated autocrine / paracrine signaling (e.g., compared to a non-cancerous control cell) . As a further example, a higher number of copies of the * gene can result in overexpression of the * protein. For example, a deregulation of a gene*, a protein*, or the expression, activity or level of any of these, may be the result of a genetic or chromosomal translocation that results in the expression of a fusion protein containing a first portion of * and a second portion of an associated (i.e., non-*) protein. In some examples, deregulation of a gene*, a protein*, or the expression, activity or level of any of these, may be the result of a genetic translocation of a gene* with another non* gene. In some embodiments, the gene *, a protein *, or the expression, activity or level of any of these is selected from the group consisting of: CD28, BCR, HER1, HER2, ΡΚΟβ, PKC0, MALT1, CARD11, CARD14 , A20, CYLD, RelB, HOIL1, NIK, regnase-1, LIMAIa, roquina-1, TRAF6, TAK1, TAB1, TAB2, TAB3, MKK7, ΙΚΚα, ΙΚΚβ, ΙΚΚγ, IkBa, p50, p65, c-Rel, JNK1 , JNK2, JNK3, MYD88 and an AP-1 transcription factor. In some embodiments, the gene* or protein* is CD28. In some embodiments, the gene * or protein * is BCR. In some embodiments, the gene * or protein * is HER1. In some embodiments, the gene* or protein* is HER2. In some embodiments, the gene* or protein* is ΡΚΟβ. In some embodiments, the gene* or protein* is PKC0. In some embodiments, the gene * or protein * is MALT1. In some embodiments, the gene* or protein* is CARD11. In some embodiments, the gene* or protein* is CARD14. In some embodiments, the gene* or protein* is A20. In some embodiments, the gene * or protein * is CYLD. In some embodiments, the gene* or protein* is RelB. In some embodiments, the gene * or protein * is HOIL1. In some embodiments, the gene * or protein * is NIK. In some embodiments, the gene* or protein* is regnase-1. In some embodiments, the gene * or protein * is LIMAIa. In some embodiments, the gene* or protein* is rochin-1. In some embodiments, the gene* or protein* is TRAF6. In some embodiments, the gene* or protein* is TAK1. In some embodiments, the gene* or protein* is TAB1. In some embodiments, the gene* or protein* is TAB2. In some embodiments, the gene* or protein* is TAB3. In some embodiments, the gene* or protein* is MKK7. In some embodiments, the gene * or protein * is ΙΚΚα. In some embodiments, the gene * or protein * is ΙΚΚβ. In some embodiments, the gene * or protein * is ΙΚΚγ. In some embodiments, the gene* or protein* is IkBa. In some embodiments, the gene* or protein* is p50. In some embodiments, the gene* or protein* is p65. In some embodiments, the gene* or protein* is c-Rel. In some embodiments, the gene* or protein* is JNK1. In some embodiments, the gene* or protein* is JNK2. In some embodiments, the gene* or protein* is JNK3. In some embodiments, the gene* or protein* is the MYD88 transcription factor. In some embodiments, the gene* or protein* is the AP-1 transcription factor. In some embodiments, a deregulation of a gene *, a protein *, or the expression, activity or level of any of these, may be a mutation in a gene * that encodes a protein * that is constitutively active or that has greater activity compared to a protein encoded by a gene * that does not include the mutation. In some QRFQCn / ZZnZ / q / ΥΙΛΙ embodiments, a higher number of copies of the * gene may result in overexpression of the * protein. In some embodiments, the gene *, protein *, or the expression, activity or level of any of these is CD28. In some embodiments, the gene *, the protein *, or the expression, activity or level of any of these is BCR. In some embodiments, the gene *, protein *, or the expression, activity or level of any of these is HER1. In some embodiments, the gene *, protein *, or the expression, activity or level of any of these is HER2. In some embodiments, the gene *, the protein *, or the expression, activity or level of any of these is ΡΚΟβ. In some embodiments, the gene *, the protein *, or the expression, activity or level of any of these is ΡΚΟΘ. In some embodiments, the gene *, protein *, or the expression, activity or level of any of these is CARD14. In some embodiments, the gene *, protein *, or the expression, activity or level of any of these is CARD9. In some embodiments, the gene *, the protein *, or the expression, activity or level of any of these is CARD10. In some embodiments, the gene *, protein *, or the expression, activity or level of any of these is CARD11. In some embodiments, the gene *, protein *, or the expression, activity or level of any of these is MALT1. As another example, a deregulation of a gene*, a protein*, or the expression, activity or level of any of these, may be a mutation in a gene* that encodes a protein* that is constitutively inactive or that has decreased activity in comparison with a protein encoded by a gene * that does not include the mutation. In some embodiments, the gene *, the protein *, or the expression, activity or level of any of these is A20. In some embodiments, the gene *, the protein *, or the expression, activity or level of any of these is CYLD. In some embodiments, the gene *, protein *, or the expression, activity or level of any of these is RelB. In some embodiments, the gene *, protein *, or the expression, activity or level of any of these is HOIL1. In some embodiments, the gene *, the protein *, or the expression, activity or level of any of these is NIK. The diseases or disorders associated with a particular gene or protein described herein refer to diseases or disorders associated with or having a deregulation of the particular gene, the particular protein, or the expression, activity or level of any (e.g., one or more) of these (e.g., any type of deregulation of the particular gene, the particular protein, or the expression, activity or level of any of these described herein). Non-limiting examples of such diseases or disorders are described herein. Likewise, the types of cancer associated with a particular gene or protein described herein refer to types of cancer associated with or having a deregulation of the particular gene, the particular protein, or the expression, activity or level of any (e.g., one or more) of these (e.g., any type of deregulation of the particular gene, the particular protein, or the expression, activity or level of any of these described herein). Non-limiting examples of such types of cancer are described herein. Example sequences of the proteins described herein are shown below. Below is an example sequence of human CD28: SEQ ID NO: 1 (UniParc Accession No. UPI0000043F4D) MLRLLLALNLFPSIQVTGNKILVKQSPMLVAYDNAVNLSCKYSYNLFSREFRASLHKGLD QRQQcn / zznz / q / υιλι SAVEVCWYGNYSQQLQVYSKTGFNCDGKLGNESVTFYLQNLYVNQTDIYFCKIEVMYPP PYLDNEKSNGTIIHVKGKHLCPSPLFPGPSKPFWVLWVGGVLACYSLLVTVAFIIFWVR SKRSRLLHSDYMNMTPRRPGPTRKHYQPYAPPRDFAAYRS Non-limiting examples of deregulation of a CD28 gene or a CD28 protein can be found, for example, in Rohr, et al., Leukemia 30.5 (2016): 1062-1070, Yoo, et al., Haematologica 101.6 (2016): 757-763, and Lee, et al., Haematologica 100.12 (2015): e505. Below is an example human BCR sequence: SEQ ID NO: 2 (UniParc Accession No. UPI000016A088) MVDPVGFAEAWKAQFPDSEPPRMELRSVGDIEQELERCKASIRRLEQEVNQERFRMIYLQ TLLAKEKKSYDRQRWGFRRAAQAPDGASEPRASASRPQPAPADGADPPPAEEPEARPDGE GSPGKARPGTARRPGAAASGERDDRGPPASVAALRSNFERIRKGHGQPGADAEKPFYVNV EFHHERGLVKVNDKEVSDRISSLGSQAMQMERKKSQHGAGSSVGDASRPPYRGRSSESSC GVDGDYEDAELNPRFLKDNLIDANGGSRPPWPP LEYQPYQSIYVGGMMEGEGKGPLLRSQ STSEQEKRLTWPRRSYSPRSFEDCGGGYTPDCSSNENLTSSEEDFSSGQSSRVSPSPTTY RMFRDKSRSPSQNSQQSFDSSSPPTPQCHKRHRHCPVVVSEATIVGVRKTGQIWPNDGEG AFHGDADGSFGTPPGYGCAADRAEEQRRHQDGLPYIDDSPSSSPHLSSKGRGSRDALVSG ALESTKASELDLEKGLEMRKWVLSGILASEETYLSHLEALLLPMKPLKAAATTSQPVLTS QQIETIFFKVPELYEIHKEFYDGLFPRVQQWSHQQRVGDLFQKLASQLGVYRAFVDNYGV AMEMAEKCCQANAQFAEISENLRARSNKDAKDPTTKNSLETLLYKPVDRVTRSTLVLHDL LKHTPASHPDHPLLQDALRISQNFLS SINEEITPRRQSMTVKKGEHRQLLKDSFMVELVE GARKLRHVFLFTDLLLCTKLKKQSGGKTQQYDCKWYIPLTDLSFQMVDELEAVPNIPLVP DEELDALKIKISQIKNDIQREKRANKGSKATERLKKKLSEQESLLLLMSPSMAFRVHSRN GKSYTFLISSDYERAEWRENIREQQKKCFRSFSLTSVELQMLTNSCVKLQTVHS IPLTIN KEDDESPGLYGFLNVIVHSATGFKQSSNLYCTLEVDSFGYFVNKAKTRVYRDTAEPNWNE EFEIELEGSQTLRILCYEKCYNKTKIPKEDGESTDRLMGKGQVQLDPQALQDRDWQRTVI AMNGIEVKLSVKFNSREFSLKRMPSRKQTGVFGVKIAWTKRERSKVPYIVRQCVEEIER RGMEEVGI YRVSGVATDIQALKAAFDVNNKDVSVMMSEMDVNAIAGTLKLYFRELPEPLF TDEFYPNFAEGIALSDPVAKESCMLNLLLSLPEANLLTFLFLLDHLKRVAEKEAVNKMSL HNLATVFGPTLLRPSEKESKLPANPSQPITMTDSWSLEVMSQVQVLLYFLQLEAIPAPDS KRQSILFSTEV Non-limiting examples of deregulation of a BCR gene or a BCR protein (e.g., a BCR-ABL fusion) can be found in, for example, Yang and Fu, Crit. Rev. Oncol. / Hematol. 93.3 (2015): 277-292, Weisberg, et al. Nat. Rev. Cancer 7.5 (2007): 345-356, and Jabbour, etal. Cancer 117.9 (2011): 1800-1811. Below is an example sequence of human HER1: SEQ ID NO: 3 (UniParc Accession No. UPI000003E750) QRQQcn / zznz / q / υιλι MRPSGTAGAALLALLAALCPASRALEEKKVCQGTSNKLTQLGTFEDHFLSLQRMFNNCEV VLGNLEITYVQRNYDLSFLKTIQEVAGYVLIALNTVERIPLENLQIIRGNMYYENSYALA VLSNYDANKTGLKELPMRNLQEILHGAVRFSNNPALCNVESIQWRDIVSSDFLSNMSMDF QNHLGSCQKCDPSCPNGSCWGAGEENCQKLTKIICAQQCSGRCRGKSPSDCCHNQCAAGC TGPRESDCLVCRKFRDEATCKDTCPPLMLYNPTTYQMDVNPEGKYSFGATCVKKCPRNYV VTDHGSCVRACGADSYEMEEDGVRKCKKCEGPCRKVCNGIGIGEFKDSLSINATNIKHFK NCTSISGDLHILPVAFRGDSFTHTPPLDPQELDILKTVKEITGFLLIQAWPENRTDLHAF ENLEIIRGRTKQHGQFSLAVVSLNITSLGLRSLKEISDGDVIISGNKNLCYANTINWKKL FGTSGQKTKIISNRGENSCKATGQVCHALCSPEGCWGPEPRDCVSCRNVSRGRECVDKCN LLEGEPREFVENSECIQCHPECLPQAMNITCTGRGPDNCIQCAHYIDGPHCVKTCPAGVM GENNTLVWKYADAGHVCHLCHPNCTYGCTGPGLEGCPTNGPKIPSIATGMVGALLLLLW ALGIGLFMRRRHIVRKRTLRRLLQERELVEPLTPSGEAPNQALLRILKETEFKKIKVLGS GAFGTVYKGLWIPEGEKVKIPVAIKELREATSPKANKEILDEAYVMASVDNPHVCRLLGI CLTSTVQLITQLMPFGCLLDYVREHKDNIGSQYLLNWCVQIAKGMNYLEDRRLVHRDLAA RNVLVKTPQHVKITDFGLAKLLGAEEKEYHAEGGKVPIKWMALESILHRIYTHQSDVWSY GVTVWELMTFGSKPYDGIPASEISSILEKGERLPQPPICTIDVYMIMVKCWMIDADSRPK FREUIEFSKMARDPQRYLVIQGDERMHLPSPTDSNFYRALMDEEDMDDWDADEYLIPQ QGFFSSPSTSRTPLLSSLSATSNNSTVACIDRNGLQSCPIKEDSFLQRYSSDPTGALTED SIDDTFLPVPEYINQSVPKRPAGSVQNPVYHNQPLNPAPSRDPHYQDPHSTAVGNPEYLN TVQPTCVNSTFDSPAHWAQKGSHQISLDNPDYQQDFFPKEAKPNGIFKGSTAENAEYLRV APQSSEFIGA Non-limiting examples of deregulation of a HER1 gene or a HER1 protein can be found, for example, in Zhang, etal., Oncotarget7.48 (2016): 78985, Ellison, etal., Journal of Clinical Pathology 66.2 (2013): 79 -89, Midha, etal., American Journal ofCancer Research 5.9 (2015): 2892, and Yamamoto, etal., Lung Cancer63.3 (2009): 315-321. Below is an example sequence of human HER2: SEQ ID NO: 4 (UniParc Accession No. UPI000003F55F) MELAALCRWGLLLALLPPGAASTQVCTGTDMKLRLPASPETHLDMLRHLYQGCQWQGNL ELTYLPTNASLSFLQDIQEVQGYVLIAHNQVRQVPLQRLRIVRGTQLFEDNYALAVLDNG DPLNNTTPVTGASPGGLRELQLRSLTEILKGGVLIQRNPQLCYQDTILWKDIFHKNNQLA LTLIDTNRSRACHPCSPMCKGSRCWGESSEDCQSLTRTVCAGGCARCKGPLPTDCCHEQC AAGCTGPKHSDCLACLHFNHSGICELHCPALVTYNTDTFESMPNPEGRYTFGASCVTACP YNYLSTDVGSCTLVCPLHNQEVTAEDGTQRCEKCSKPCARVCYGLGMEHLREVRAVTSAN IQEFAGCKKIFGSLAFLPESFDGDPASNTAPLQPEQLQVFETLEEITGYLYISAWPDSLP DLSVFQNLQVIRGRILHNGAYSLTLQGLGISWLGLRSLRELGSGLALIHHNTHLCFVHTV PWDQLFRNPHQALLHTANRPEDECVGEGLACHQLCARGHCWGPGPTQCVNCSQFLRGQEC VEECRVLQGLPREYVNARHCLPCHPECQPQNGSVTCFGPEADQCVACAHYKDPPFCVARC PSGVKPDLSYMPIWKFPDEEGACQPCPINCTHSCVDLDDKGCPAEQRASPLTSIISAWG ILLWVLGWFGILIKRRQQKIRKYTMRRLLQETELVEPLTPSGAMPNQAQMRILKETEL RKVKVLGSGAFGTVY KGIWIPDGENVKIPVAIKVLRENTSPKANKEILDEAYVMAGVGSP YVSRLLGICLTSTVQLVTQLMPYGCLLDHVRENRGRLGSQDLLNWCMQIAKGMSYLEDVR LVHRDLAARNVLVKSPNHVKITDFGLARLLDIDETEYHADGGKVPIKWMALESILRRRFT HQSDVWSYGVTVWELMTFGAKPYDGIPAREIPDLLEKGERLPQPPICTIDVYMIMVKCWM IDSECRPRFRELVSEFSRMARDPQ RFVVIQNEDLGPASPLDSTFYRSLLEDDDMGDLVDA EEYLVPQQGFFCPDPAPGAGGMVHHRHRSSSTRSGGGDLTLGLEPSEEEAPRSPLAPSEG AGSDVFDGDLGMGAAKGLQSLPTHDPSPLQRYSEDPTVPLPSETDGYVAPLTCSPQPEYV NQPDVRPQPPSPREGPLPAARPAGATLERPKTLSPGKNGWKDVFAFGGAVENPEYLT PQ GGAAPQPHPPPAFSPAFDNLYYWDQDPPERGAPPSTFKGTPTAENPEYLGLDVPV Non-limiting examples of deregulation of a HER2 gene or a HER2 protein can be found, for example, in Petrelli, Fausto, etal., Breast Cancer Research and Treatment 166.2 (2017): 339-349, Yan, etal., Cancer and Metastasis Reviews 34.1 (2015): 157-164, Koshkin, etal., BladderCancer5.1 (2019): 1-12, and Connell, etal., ESMO Open 2.5 (2017). As used herein, the term cancer associated with a signal transducer between a cell surface receptor and a CBM complex refers to types of cancer associated with or having a deregulation of a gene, protein, or expression. , activity or level of any (e.g., one or more) of these associated with a signal transducer between a cell surface receptor and a CBM complex. In some embodiments, a cancer type associated with a signal transducer between a cell surface receptor and a CBM complex is selected from the group consisting of a PKC3-associated cancer type, a PCK9-associated cancer type and a combination of these. The types of cancer associated with a particular gene or protein described in this paragraph refer to types of cancer associated with or having a dysregulation of the particular gene, the particular protein, or the expression, activity or level of either ( for example, one or more) of these (for example, any type of deregulation of the particular gene, the particular protein, or the expression, activity or level of any of these described herein). Non-limiting examples of such types of cancer are described herein. Below is an example sequence of human ΡΚΟβ: SEQ ID NO: 5 (UniParc Accession No. UPI000012DF67) MADPAAGPPPSEGEESTVRFARKGALRQKNVHEVKNHKFTARFFKQPTFCSHCTDFIWGF GKQGFQCQVCCFWHKRCHEFVTFSCPGADKGPASDDPRSKHKFKIHTYSSPTFCDHCGS LLYGLIHQGMKCDTCMMNVHKRCVMNVPSLCGTDHTERRGRIYIQAHIDRDVLIVLVRDA KNLVPMDPNGLSDPYVKLKLIPDPKSES KQKTKTIKCSLNPEWNETFRFQLKESDKDRRL SVEIWDWDLTSRNDFMGSLSFGISELQKASVDGWFKLLSQEEGEYFNVPVPPEGSEANEE LRQKFERAKISQGTKVPEEKTTNTVSKFDNNGNRDRMKLTDFNFLMVLGKGSFGKVMLSE RKGTDELYAVKILKKDWIQDDDVECTMVEKRVLALPGKPPFLTQ LHSCFQTMDRLYFVM EYVNGGDLMYHIQQVGRFKEPHAVFYAAEIAIGLFFLQSKGIIYRDLKLDNVMLDSEGHI KIADFGMCKENIWDGVTTKTFCGTPDYIAPEIIAYQPYGKSVDWWAFGVLLYEMLAGQAP FEGEDEDELFQSIMEHNVAYPKSMSKEAVAICKGLMTKHPGKRLGCGPEGERDIKEHAFF RYIDWEKLERK EIQPPYKPKARDKRDTSNFDKEFTRQPVELTPTDKLFIMNLDQNEFAGF SYTNPEFVINV Below is an example sequence of human PKC0: SEQ ID NO: 6 (UniParc Accession No. UPI000012DF74) MSPFLRIGLSNFDCGSCQSCQGEAVNPYCAVLVKEYVESENGQMYIQKKPTMYPPWDSTF DAHINKGRVMQIIVKGKNVDLISETTVELYSLAERCRKNNGKTEIWLELKPQGRMLMNAR YFLEMSDTKDMNEFETEGFFALHQRRGAIKQAKVHHVKCHEFTATFFPQPTFCSVCHEFV WGLNKQGYQCRQCNAAIHKKCIDKVIAKCTGSAINSRETMFHKERFKIDMPHRFKVYNYK SPTFCEHCGTLLWGLARQGL KCDACGMNVHHRCQTKVANLCGINQKLMAEALAMIESTQQ ARCLRDTEQIFREGPVEIGLPCSIKNEARPPCLPTPGKREPQGISWESPLDEVDKMCHLP EPELNKERPSLQIKLKIEDFILHKMLGKGSFGKVFLAEFKKTNQFFAIKALKKDVVLMDD DVECTMVEKRVLSLAWEHPFLTHMFCTFQTKENLFFVMEYLNGGDLMYHIQSCHKFDLSR ATFYAAEIILGLQFLHSKGIVYRDLKLDNILLDKDGHIKIADFGMCKENMLGDAKTNTFC GTPDYIAPEILLGQKYNHSVDWWSFGVLLYEMLIGQSPFHGQDEEELFHSIRMDNPFYPR WLEKEAKDLLVKLFV REPEKRLGVRGDIRQHPLFREINWEELERKEIDPPFRPKVKSPFD CSNFDKEFLNEKPRLSFADRALINSMDQNMFRNFSFMNPGMERLIS As used herein, the term "component of a cancer type associated with a CBM complex" refers to cancer types associated with or having a deregulation of a gene, a protein, or the expression, activity or level of either ( for example, one or more) of these associated with a component of a CBM complex. In some embodiments, a component of a type of cancer associated with the CBM complex is selected from the group consisting of a type of cancer associated with MALT1, a type of cancer associated with CARD11, a type of cancer associated with CARD14, a type of CARD10-associated cancer, a type of CARD9-associated cancer, a type of BCL10-associated cancer and combinations of these. In some embodiments, a CBM complex-associated cancer type is selected from the group consisting of a MALT 1-associated cancer type, a CARD11-associated cancer type, a BCL10-associated cancer type, and combinations thereof. The types of cancer associated with a particular gene or protein described in this paragraph refer to types of cancer associated with or having a dysregulation of the particular gene, the particular protein, or the expression, activity or level of either ( for example, one or more) of these (for example, any type of deregulation of the particular gene, the particular protein, or the expression, activity or level of any of these described herein). Non-limiting examples of such types of cancer are described herein. As used herein, the term MALT1-associated autoimmune disorder refers to autoimmune disorders associated with, or having, a deregulation of a MALT1 gene, a MALT1 protein (also referred to herein as MALT1 protease protein or MALT1 protease), or the expression, activity or level of any QRQQcn / zznz / q / υιλι (for example, one or more) of these (for example, any type of deregulation of a MALT 1 gene, a MALT1 protease, a MALT1 protease domain, or the expression, activity or level of any of these described herein). Non-limiting examples of MALT1-associated autoimmune disorders are described herein. As used herein, the term MALT1-associated inflammatory disorder refers to inflammatory disorders associated with, or having, a deregulation of a MALT1 gene, a MALT1 protein (also referred to herein as MALT1 protease protein or MALT1 protease), or the expression, activity or level of any (for example, one or more) of these (for example, any type of deregulation of a MALT 1 gene, a MALT 1 protease, a MALT1 protease domain, or the expression, activity or level of any of these described herein). Non-limiting examples of MALT1-associated inflammatory disorders are described herein. As used herein, the term MALT1-associated cancer refers to types of cancer associated with, or having, a deregulation of a MALT1 gene, a MALT1 protein (also referred to herein as MALT1 protease protein or MALT1 protease), or the expression, activity or level of any (for example, one or more) of these (for example, any type of deregulation of a MALT1 gene, a MALT1 protein, a MALT1 protease domain, or the expression, activity or level of any of these described herein). Non-limiting examples of a type of cancer associated with MALT 1 are described herein. The phrase deregulation of a MALT1 gene, a MALT1 protein, or the expression, activity or level of any of these refers to a genetic mutation (for example, a chromosomal translocation that results in the expression of a fusion protein that includes a MALT1 protease domain and a fusion component, a mutation in a MALT1 gene that results in the expression of a MALT1 protein that includes a deletion of at least one amino acid compared to a wild-type MALT1 protein, a mutation in a gene MALT1 resulting in the expression of a MALT1 protein with one or more point mutations compared to a wild-type MALT1 protein, a mutation in a MALT1 gene resulting in the expression of a MALT1 protein with at least one amino acid inserted in compared to a wild-type MALT1 protein, a gene duplication that results in a higher level of MALT1 protein in a cell or a mutation in a regulatory sequence (e.g., a promoter and / or enhancer) that results in a higher level of MALT 1 protein in a cell), an alternatively spliced ​​version of a MALT1 mRNA that results in a MALT1 protein that has a deletion of at least one amino acid in the MALT 1 protein compared to the wild-type MALT 1 protein or increased expression (e.g., increased levels) of a wild-type MALT1 protein in a mammalian cell due to abnormal cellular signaling and / or dysregulated autocrine / paracrine signaling (e.g., compared to a non-cancerous control cell ). As another example, a deregulation of a MALT1 gene, a MALT1 protein, or the expression, activity or level of any of these, may be a mutation in a MALT1 gene that encodes a MALT1 protein that is constitutively active or that has increased activity in comparison with a protein encoded by a MALT 1 gene that does not include the mutation. As a further example, increased copy numbers of the MALT 1 gene can result in overexpression of the MALT1 protease. For example, a deregulation of a MALT1 gene, a MALT1 protein, or the expression, activity or level of any of these, may be the result of a genetic or chromosomal translocation that results in the expression of a fusion protein containing a first portion of MALT1 that includes a functional protease domain and a second portion of an associated protein (i.e., not MALT1). In some examples, deregulation of a MALT1 gene, a MALT1 protein, or the expression, activity or level of any of these, may be the result of a genetic translocation of a MALT1 gene with another non-MALT1 gene. Below is an example sequence of human MALT1: SEQ ID NO: 7 (UniParc Accession No. UPI000004D05E) MSLLGDPLQALPPSAAPTGPLLAPPAGATLNRLREPLLRRLSELLDQAPEGRGWRRLAEL AGSRGRLRLSCLDLEQCSLKVLEPEGSPSLCLLKLMGEKGCTVTELSDFLQAMEHTEVLQ LLSPPGIKITVNPESKAVLAGQFVKLCCRATGHPFVQYQWFKMNKEIPNGNTSELIFNAV HVKDAGFYVCRVNNNFTFEFSQWSQLDVCDIPESFQRSVDGVSESKLQICVEPTSQKLMP GSTLVLQCVAVGSPIPHYQWF KNELPLTHETKKLYMVPYVDLEHQGTYWCHVYNDRDSQD SKKVEIIIGRTDEAVECTEDELNNLGHPDNKEQTTDQPLAKDKVALLIGNMNYREHPKLK APLVDVYELTNLLRQLDFKWSLLDLTEYEMRNAVDEFLLLLDKGVYGLLYYAGHGYENF GNSFMVPVDAPNPYRSENCLCVQNILKLMQEKETGLNVFL LDMCRKRNDYDDTIPILDAL KVTANIVFGYATCQGAEAFEIQHSGLANGIFMKFLKDRLLEDKKITVLLDEVAEDMGKCH LTKGKQALEIRSSLSEKRALTDPIQGTEYSAESLVRNLQWAKAHELPESMCLKFDCGVQI QLGFAAEFSNVMIIYTSIVYKPPEIIMCDAYVTDFPLDLDIDPKDANKGTPEETGSYLVS KDLPKHCLY TRLSSLQKLKEHLVFTVCLSYQYSGLEDTVEDKQEVNVGKPLIAKLDMHRG LGRKTCFQTCLMSNGPYQSSAATSGGAGHYHSLQDPFHGVYHSHPGNPSNVTPADSCHCS RTPDAFISSFAHHASCHFSRSNVPVETTDEIPFSFSDRLRISEK Non-limiting examples of deregulation of a MALT1 gene or a MALT1 protein are shown in Table B1 below. Table B1. QRQQcn / zznz / q / υιλι MALT1 protein amino acid substitutions / insertions / deletions Amino acid positions Non-limiting example mutations Non-limiting example MALT1-associated cancers 717 M717I4 MALT fusion components Non-limiting example MALT1- fusion component Associated cancer(s) (s) BIRC3 (also called IAP2; CIAP2; and API2)1 Diffuse large B-cell lymphoma (DLBCL)1; Extranodal low-grade MALT lymphoma2 IGH ABC-DLBCL2 SEC11C Breast cancer3 1US Patent US 10,711,036 US Patent Application Publication US20190160045A1 US Patent Application Publication US20130096021A1 US Patent Application Publication US20150320754A1 As used herein, the term "CARD11-associated autoimmune disorder" refers to autoimmune disorders associated with, or having, a deregulation of a CARD11 gene, a CARD11 protein, or the expression, activity or level of either (e.g. one or more) of these (for example, any of the types of deregulation of a CARD11 gene, a CARD11 protein, or the expression, activity or level of any of these described herein). As used herein, the term CARD11-associated inflammatory disorder refers to inflammatory disorders associated with, or having, a deregulation of a CARD11 gene, a CARD11 protein, or the expression, activity or level of either (e.g. one or more) of these (for example, any of the types of deregulation of a CARD11 gene, a CARD11 protein, or the expression, activity or level of any of these described herein). As used herein, the term CARD11-associated cancer refers to types of cancer associated with, or having, a deregulation of a CARD11 gene, a CARD11 protein, or the expression, activity or level of either (e.g. one or more) of these (for example, any of the types of deregulation of a CARD11 gene, a CARD11 protein, or the expression, activity or level of any of these described herein). Non-limiting examples of a type of cancer associated with CARD11 are described herein. The phrase deregulation of a CARD11 gene, a CARD11 protein, or the expression, activity or level of any of these refers to a genetic mutation (for example, a chromosomal translocation that results in the expression of a fusion protein that includes a CARD11 domain and a fusion component, a mutation in a CARD11 gene that results in the expression of a CARD11 protein that includes a deletion of at least one amino acid compared to a wild-type CARD11 protein, a mutation in a CARD11 gene that results in the expression of a CARD11 protein with one or more point mutations compared to a wild-type CARD11 protein, a mutation in a CARD11 gene that results in the expression of a CARD11 protein with at least one amino acid inserted compared to a wild-type CARD11 protein, a gene duplication resulting in an increased level of CARD11 protein in a cell, or a mutation in a regulatory sequence (e.g., a promoter and / or enhancer) resulting in an increased level of CARD11 protein in a cell), an alternatively spliced ​​version of a CARD11 mRNA that results in a CARD11 protein that has a deletion of at least one amino acid in the CARD11 protein compared to the wild-type CARD11 protein or increased expression (for For example, increased levels) of a wild-type CARD11 protein in a mammalian cell due to abnormal cell signaling and / or deregulated autocrine / paracrine signaling (for example, compared to a non-cancerous control cell). As another example, a deregulation of a CARD11 gene, a CARD11 protein, or the expression, activity or level of any of these, may be a mutation in a CARD11 gene. QRFQCn / ZZnZ / q / ΥΙΛΙ that encodes a CARD11 protein that is constitutively active or that has greater activity compared to a protein encoded by a CARD11 gene that does not include the mutation. As a further example, an increased number of copies of the CARD11 gene can result in overexpression of the CARD11 protein. For example, a deregulation of a CARD11 gene, a CARD11 protein, or the expression, activity or level of any of these, may be the result of a genetic or chromosomal translocation that results in the expression of a fusion protein containing a first portion of CARD11 and a second portion of an associated protein (i.e., not CARD11). In some examples, deregulation of a CARD11 gene, a CARD11 protein, or the expression, activity or level of any of these, may be the result of a genetic translocation of a CARD11 gene with another non-CARD11 gene. Below is an example sequence of human CARD11: SEQ ID NO: 8 (UniParc Accession No. UPI00003FED38) MPGGGPEMDDYMETLKDEEDALWENVECNRHMLSRYINPAKLTPYLRQCKVIDEQDEDEV LNAPMLPSKINRAGRLLDILHTKGQRGYWFLESLEFYYPELYKLVTGKEPTRRFSTIW EEGHEGLTHFLMNEVIKLQQQMKAKDLQRCELLARLRQLEDEKKQMTLTRVELLTFQERY YKMKEERDSYNDELVKVKDDNYNL AMRYAQLSEEKNMAVMRSRDLQLEIDQLKHRLNKME EECKLERNQSLKLKNDIENRPKKEQVLELERENEMLKTKNQELQSIIQAGKRSLPDSDKA ILDILEHDRKEALEDRQELVNRIYNLQEEARQAEELRDKYLEEKEDLELKCSTLGKDCEM YKHRMNTVMLQLEEVERERDQAFHSRDEAQTQYSQCLIEKDK YRKQIRELEEKNDEMRIE MVRREACIVNLESKLRRLSKDSNNLDQSLPRNLPVTIISQDFGDASPRTNGQEADDSSTS EESPEDSKYFLPYHPPQRRMNLKGIQLQRAKSPISLKRTSDFQAKGHEEEGTDASPSSCG SLPITNSFTKMQPPRSRSSIMSITAEPPGNDSIVRRYKEDAPHRSTVEEDNDSGGFDALD LDDDSHERYSFG PSSIHSSSSSHQSEGLDAYDLEQVNLMFRKFSLERPFRPSVTSVGHVR GPGPSVQHTTLNGDSLTSQLTLLGNARGSFVHSVKPGSLAEKAGLREGHQLLLEGCIR GERQSVPLDTCTKEEAHWTIQRCSGPVTLHYKVNHEGYRKLVKDMEDGLITSGDSFYIRL NLNISSQLDACTMSLKCDDWHVRDTMYQDRHEWLCAR VDPFTDHDLDMGTIPSYSRAQQ LLLVKLQRLMHRGSREEVDGTHHTLRALRNTLQPEEALSTSDPRVSPRLSRASFLFGQLL QFVSRSENKYKRMNSNERVRIISGSPLGSLARSSLDATKLLTEKQEELDPESELGKNLSL IPYSLVRAFYCERRRPVLFTPTVLAKTLVQRLLNSGGAMEFTICKSDIVTRDEFLRRQKT ETIIYSREKNPNAFECIAPAN IEAVAAKNKHCLLEAGIGCTRDLIKSNIYPIVLFIRVCE KNIKRFRKLLPRPETEEEFLRVCRLKEKELEALPCLYATVEPDMWGSVEELLRWKDKIG EEQRKTIWVDEDQL Non-limiting examples of deregulation of a CARD11 gene or a CARD11 protein are shown in Table B2 below. QRFQCn / ZZnZ / q / ΥΙΛΙ Table B2. Amino acid substitutions / insertions / deletions of the CARD11 protein Amino acid positions Non-limiting example mutations Non-limiting example CARD11-associated cancer types 47 R47C2 Cutaneous squamous cell carcinoma2 123 G123S1 Lymphoma1 126 G126D1 Lymphoma1 130 F130V2 Cutaneous squamous cell carcinoma2 167 T167M2 Cutaneous squamous cell carcinoma2 215 K215M, K215N1 Lymphoma1 230 D230N1 Lymphoma1 357 D357E1 Lymphoma1 360 M360V1 Lymphoma1 361 Y361C1 Lymphoma1 368 V368I2 Cutaneous squamous cell carcinoma2 737 H737 L2 Cutaneous squamous cell carcinoma2 750 H750R2 Cutaneous squamous cell carcinoma2 833 P833L2 Cutaneous squamous cell carcinoma squamous cell carcinoma2 900 L900F2 Cutaneous squamous cell carcinoma2 1015 L1015F2 Cutaneous squamous cell carcinoma2 1016 R1016L2 Cutaneous squamous cell carcinoma2 1085 R1085S2 Cutaneous squamous cell carcinoma2 1086 F1086S2 Cutaneous squamous cell carcinoma2 1Wu, ef al., Oncotarget 7.25 (2016): 38180. 2Watt, et al. The American Journal of Pathology 185.9 (2015): 2354-2363. As used herein, the term "CARD14-associated autoimmune disorder" refers to autoimmune disorders associated with, or having, a deregulation of a CARD14 gene, a CARD14 protein, or the expression, activity or level of either (e.g. one or more) of these (for example, any of the types of deregulation of a CARD14 gene, a CARD14 protein, or the expression, activity or level of any of these described herein). As used herein, the term CARD14-associated inflammatory disorder refers to inflammatory disorders associated with, or having, a deregulation of a CARD14 gene, a CARD14 protein, or the expression, activity or level of either (e.g. one or more) of these (for example, any of the types of deregulation of a gene QAFQCn / ZZnZ / q / ΥΙΛΙ CARD14, a CARD14 protein, or the expression, activity or level of any of these described herein). As used herein, the term CARD14-associated cancer refers to types of cancer associated with, or having, a deregulation of a CARD14 gene, a CARD14 protein, or the expression, activity or level of either (e.g. one or more) of these (for example, any of the types of deregulation of a CARD14 gene, a CARD14 protein, or the expression, activity or level of any of these described herein). Below is an example sequence of human CARD14: SEQ ID NO: 9 (UniParc Accession No. UPI000013D81B) MGELCRRDSALTALDEETLWEMMESHRHRIVRCICPSRLTPYLRQAKVLCQLDEEEVLHS PRLTNSAMRAGHLLDLLKTRGKNGAIAFLESLKFHNPDVYTLVTGLQPDVDFSNFSGLME TSKLTECLAGAIGSLQEELNQEKGQKEVLLRRCQQLQEHLGLAETRAEGLHQLEADHSRM KREVSAHFHEVLRLKDEMLSLSLHYSNALQEKELAASRCRSLQEELYLLKQELQRANMVS SCELELQEQSLRTASDQESG DEELNRLKEENEKLRSLTFSLAEKDILEQSLDEARGSRQE LVERIHSLRERAVAAERQREQYWEEKEQTLLQFQKSKMACQLYREKVNALQAQVCELQKE RDQAYSARDSAQREISQSLVEKDSLRRQVFELTDQVCELRTQLRQLQAEPPGVLKQEART REPCPREKQRLVRMHAICPRDDSDCSLVS STESQLLSDLSATSSRELVDSFRSSSPAPPS QQSLYKRVAEDFGEEPWSFSSCLEIPEGDPGALPGAKAGDPHLDYELLDTADLPQLESSL QPVSPGRLDVSESGVLMRRRPARRILSQVTMLAFQGDALLEQISVIGGNLTGIFIHRVTP GSAADQMALRPGTQIVMVDYEASEPLFKAVLEDTTLEEAVGLLRRVDGFCCLSVKVNTDG YKRLLQDLEAK VATSGDSFYIRVNLAMEGRAKGELQVHCNEVLHVTDTMFQGCGCWHAHR VNSYTMKDTAAHGTIPNYSRAQQQLIALIQDMTQQCTVTRKPSSGGPQKLVRIVSMDKAK ASPLRLSFDRGQLDPSRMEGSTCFWAESCLTLVPYTLVRPHRPARPRPVLLVPRAVGKI LSEKLCLLQGFKKCLAEYLSQEEYEAWSQRGDII QEGEVSGGRCWVTRHAVESLMEKNTH ALLDVQLDSVCTLHRMDIFPIVIHVSVNEKMAKKLKKGLQRLGTSEEQLLEAARQEEGDL DRAPCLYSSLAPDGWSDLDGLLSCVRQAIADEQKKWWTEQSPR As used herein, the term "CARD10-associated autoimmune disorder" refers to autoimmune disorders associated with, or having, a deregulation of a CARD10 gene, a CARD10 protein, or the expression, activity or level of either (e.g. one or more) of these (for example, any of the types of deregulation of a CARD10 gene, a CARD10 protein, or the expression, activity or level of any of these described herein). As used herein, the term CARD10-associated inflammatory disorder refers to inflammatory disorders associated with, or having, a dysregulation of a CARD10 gene, a CARD10 protein, or the expression, activity or level of either (e.g. one or more) of these (for example, any of the types of deregulation of a CARD10 gene, a CARD10 protein, or the expression, activity or level of any of these described herein). As used herein, the term CARD10-associated cancer refers to types of cancer associated with, or having, a deregulation of a CARD10 gene, a CARD10 protein, or the expression, activity or level of either (e.g. one or more) of these (for example, any of the types of deregulation of a CARD10 gene, a CARD10 protein, or the expression, activity or level of any of these described herein). The phrase deregulation of a CARD10 gene, a CARD10 protein, or the expression, activity or level of any of these refers to a genetic mutation (for example, a chromosomal translocation that results in the expression of a fusion protein that includes a CARD10 domain and a fusion component, a mutation in a CARD10 gene that results in the expression of a CARD10 protein that includes a deletion of at least one amino acid compared to a wild-type CARD10 protein, a mutation in a CARD10 gene that results in the expression of a CARD10 protein with one or more point mutations compared to a wild-type CARD10 protein, a mutation in a CARD10 gene that results in the expression of a CARD10 protein with at least one amino acid inserted compared to a wild-type CARD10 protein, a gene duplication resulting in an increased level of CARD10 protein in a cell, or a mutation in a regulatory sequence (e.g., a promoter and / or enhancer) resulting in an increased level of CARD10 protein in a cell), an alternatively spliced ​​version of a CARD10 mRNA that results in a CARD10 protein that has a deletion of at least one amino acid in the CARD10 protein compared to the wild-type CARD10 protein or increased expression (for For example, increased levels) of a wild-type CARD10 protein in a mammalian cell due to abnormal cell signaling and / or deregulated autocrine / paracrine signaling (for example, compared to a non-cancerous control cell). As another example, a deregulation of a CARD10 gene, a CARD10 protein, or the expression, activity or level of any of these, may be a mutation in a CARD10 gene that encodes a CARD10 protein that is constitutively active or that has increased activity in comparison with a protein encoded by a CARD10 gene that does not include the mutation. As a further example, an increased number of copies of the CARD10 gene can result in overexpression of the CARD10 protein. For example, a deregulation of a CARD10 gene, a CARD10 protein, or the expression, activity or level of any of these, may be the result of a genetic or chromosomal translocation that results in the expression of a fusion protein containing a first portion of CARD10 and a second portion of an associated protein (i.e., not CARD10). In some examples, deregulation of a CARD10 gene, a CARD10 protein, or the expression, activity or level of any of these, may be the result of a genetic translocation of a CARD10 gene with another non-CARD10 gene. Below is an example sequence of human CARD10: SEQ ID NO: 10 (UniParc Accession No. UPI0000044645) MPGRAEAGEAEEEAGAGSGSEAEEDALWERIEGVRHRLARALNPAKLTPYLRQCRVIDEQ DEEEVLSTYRFPCRVNRTGRLMDILRCRGKRGYEAFLEALEFYYPEHFTLLTGQEPAQRC SMILDEEGPEGLTQFLMTEVRRLREARKSQLQREQQLQARGRVLEEERAGLEQRLRDQQQ AQERCQRLREDWEAGSLELLRLKDENYMIAMRLAQLS EEKNSAVLRSRDLQLAVDQLKLK VSRLEEECALLRRARGPPPGAEEKEKEKEKEKEPDNVDLVSELRAENQRLTASLRELQEG LQQEASRPGAPGSERILLDILEHDWREAQDSRQELCQKLHAVQGELQWAEELRDQYLQEM EDLRLKHRTLQKDCDLYKHRMATVLAQLEEIEKERDQAIQSRDRIQLQYSQSLIEKDQYR KQVRGLEAERDELLTTLTSLEGTKALLEVQLQRAQGGTCLKACASSHSLCSNLSSTWSLS EFPSPLGGPEATGEAAVMGGPEPHNSEEATDSEKEINRLSILPFPPSAGSILRRQREEDP APPKRSFSSMSDITGSVTLKPWSPGLS SSSSSDSVWPLGKPEGLLARGCGLDFLNRSLAI RVSGRSPPGGPEPQDKGPDGLSFYGDRWSGAWRRVLSGPGSARMEPREQRVEAAGLEGA CLEAEAQQRTLLWNQGSTLPSLMDSKACQSFHEALEAWAKGPGAEPFYIRANLTLPERAD PHALCVKAQEILRLVDSAYKRRQEWFCTRVDPLTLRDLDRGTVPNYQRAQQLLEVQ EKCL PSSRHRGPRSNLKKRALDQLRLVRPKPVGAPAGDSPDQLLLEPCAEPERSLRPYSLVRPL LVSALRPWLLPECLAPRLIRNLLDLPSSRLDFQVCPAESLSGEELCPSSAPGAPKAQPA TPGLGSRIRAIQESVGKKHCLLELGARGVRELVQNEIYPIVIHVEVTEKNVREVRGLLGR PGWRDSELLRQCRGSEQVLWGLPCSWVQVPAHEWGHAEELAKWRGRILQEQARLVWVEC GSSRGCPSSSEA As used herein, the term "CARD9-associated autoimmune disorder" refers to autoimmune disorders associated with, or having, a deregulation of a CARD9 gene, a CARD9 protein, or the expression, activity or level of either (e.g. one or more) of these (for example, any type of deregulation of a CARD9 gene, a CARD9 protein, or the expression, activity or level of any of these described herein). As used herein, the term "CARD9-associated inflammatory disorder" refers to inflammatory disorders associated with, or having, a deregulation of a CARD9 gene, a CARD9 protein, or the expression, activity or level of either (e.g. one or more) of these (for example, any type of deregulation of a CARD9 gene, a CARD9 protein, or the expression, activity or level of any of these described herein). As used herein, the term CARD9-associated cancer refers to types of cancer associated with, or having, a deregulation of a CARD9 gene, a CARD9 protein, or the expression, activity or level of either (e.g. one or more) of these (for example, any type of deregulation of a CARD9 gene, a CARD9 protein, or the expression, activity or level of any of these described herein). The phrase deregulation of a CARD9 gene, a CARD9 protein, or the expression, activity or level of any of these refers to a genetic mutation (for example, a chromosomal translocation that results in the expression of a fusion protein that includes a CARD9 domain and a fusion component, a mutation in a CARD9 gene that results in the expression of a CARD9 protein that includes a deletion of at least one amino acid compared to a wild-type CARD9 protein, a mutation in a CARD9 gene that results in the expression of a CARD9 protein with one or more point mutations compared to a wild-type CARD9 protein, a mutation in a CARD9 gene that results in the expression of a CARD9 protein with at least one amino acid inserted compared to a wild-type CARD9 protein, a gene duplication resulting in an increased level of CARD9 protein in a cell, or a mutation in a regulatory sequence (e.g., a promoter and / or enhancer) resulting in an increased level of CARD9 protein in a cell), an alternatively spliced ​​version of a CARD9 mRNA that results in a CARD9 protein that has a deletion of at least one amino acid in the CARD9 protein compared to the wild-type CARD9 protein or increased expression (for For example, increased levels) of a wild-type CARD9 protein in a mammalian cell due to abnormal cell signaling and / or deregulated autocrine / paracrine signaling (for example, compared to a non-cancerous control cell). As another example, a deregulation of a CARD9 gene, a CARD9 protein, or the expression, activity or level of any of these, may be a mutation in a CARD9 gene that encodes a CARD9 protein that is constitutively active or that has increased activity in comparison with a protein encoded by a CARD9 gene that does not include the mutation. As a further example, an increased number of copies of the CARD9 gene can result in overexpression of the CARD9 protein. For example, a deregulation of a CARD9 gene, a CARD9 protein, or the expression, activity or level of any of these, may be the result of a genetic or chromosomal translocation that results in the expression of a fusion protein containing a first portion of CARD9 and a second portion of an associated protein (i.e., not CARD9). In some examples, deregulation of a CARD9 gene, a CARD9 protein, or the expression, activity or level of any of these, may be the result of a genetic translocation of a CARD9 gene with another non-CARD9 gene. Below is an example sequence of human CARD9: SEQIDNO: 11 (UniParc Accession No. UPI000013E4EB) MSDYENDDECWSVLEGFRVTLTSVIDPSRITPYLRQCKVLNPDDEEQVLSDPNLVIRKRK VGVLLDILQRTGHKGYVAFLESLELYYPQLYKKVTGKEPARVFSMIIDASGESGLTQLLM TEVMKLQKKVQDLTALLSSKDDFIKELRVKDSLLRKHQERVQRLKEECEAGSRELKRCKE ENYDLAMRLAHQSEEKGAALMR NRDLQLEIDQLKHSLMKAEDDCKVERKHTLKLRHAMEQ RPSQELLWELQQEKALLQARVQELEASVQEGKLDRSSPYIQVLEEDWRQALRDHQEQANT IFSLRKDLRQGEARRLRCMEEKEMFELQCLALRKDSKMYKDRIEAILLQMEEVAIERDQA IATREELHAQHARGLQEKDALRKQVRELGEKADELQL QVFQCEAQKEYGRLRRQQLET LVLSSDLEDGSPRRSQELSLPQDLEDTQLSDKGCLAGGGSPKQPFAALHQEQVLRNPHDA GLSSGEPPEKERRRLKESFENYRRKRALRKMQKGWRQGEEDRENTTGSDNTDTEGS As used herein, the term "BCL10-associated autoimmune disorder" refers to autoimmune disorders associated with, or having, a deregulation of a BCL10 gene, a BCL10 protein, or the expression, activity or level of either (e.g. one or more) of these (for example, any of the types of deregulation of a BCL10 gene, a BCL10 protein, or the expression, activity or level of any of these described herein). As used herein, the term "BCL10-associated inflammatory disorder" refers to inflammatory disorders associated with, or having, a deregulation of a BCL10 gene, a BCL10 protein, or the expression, activity or level of either (e.g. one or more) of these (for example, any of the types of deregulation of a BCL10 gene, a BCL10 protein, or the expression, activity or level of any of these described herein). As used herein, the term BCL10-associated cancer refers to types of cancer associated with, or having, a deregulation of a BCL10 gene, a BCL10 protein, or the expression, activity or level of either (e.g. one or more) of these (for example, any type of deregulation of a BCL10 gene, a protein QRQQcn / zznz / q / υιλι BCL10, or the expression, activity or level of any of these described herein). The phrase deregulation of a BCL10 gene, a BCL10 protein, or the expression, activity or level of any of these refers to a genetic mutation (for example, a chromosomal translocation that results in the expression of a fusion protein that includes a BCL10 domain and a fusion component, a mutation in a BCL10 gene that results in the expression of a BCL10 protein that includes a deletion of at least one amino acid compared to a wild-type BCL10 protein, a mutation in a BCL10 gene that results resulting in the expression of a BCL10 protein with one or more point mutations compared to a wild-type BCL10 protein, a mutation in a BCL10 gene resulting in the expression of a BCL10 protein with at least one inserted amino acid compared to a wild-type BCL10 protein, a gene duplication that results in a higher level of BCL10 protein in a cell, or a mutation in a regulatory sequence (e.g., a promoter and / or enhancer) that results in a higher level of protein BCL10 in a cell), an alternatively spliced ​​version of a BCL10 mRNA that results in a BCL10 protein that has a deletion of at least one amino acid in the BCL10 protein compared to the wild-type BCL10 protein or increased expression (e.g. , higher levels) of a wild-type BCL10 protein in a mammalian cell due to abnormal cell signaling and / or deregulated autocrine / paracrine signaling (e.g., compared to a non-cancerous control cell). For example, a deregulation of a BCL10 gene, a BCL10 protein, or the expression, activity or level of any of these, may be the result of a genetic or chromosomal translocation that results in the expression of a fusion protein containing a first portion of BCL10 and a second portion of an associated protein (i.e., not BCL10). In some examples, deregulation of a BCL10 gene, a BCL10 protein, or the expression, activity or level of any of these, may be the result of a genetic translocation of a BCL10 gene with another non-BCL10 gene. Below is an example sequence of human BCL10: SEQ ID NO: 12 (UniParc Accession No. UPI000012682F) MEPTAPSLTEEDLTEVKKDALENLRVYLCEKIIAERHFDHLRAKKILSREDTEEISCRTS SRKRAGKLLDYLQENPKGLDTLVESIRREKTQNFLIQKITDEVLKLRNIKLEHLKGLKCS SCEPFPDGATNNLSRSNSDESNFSEKLRASTVMYHPEGESSTTPFSTNSSLNLPVLEVG RTENTIFSSTTLPRPGDPGAPPLPPDLQLEEEGTCANSSE MFLPLRSRTVSRQ Non-limiting examples of deregulation of a BCL10 gene or a BCL10 protein are shown in Table B3 below. Table B3. Amino acid substitutions / insertions / deletions of the BCL10 protein Amino acid positions Non-limiting example mutations Non-limiting example BCL10-associated cancer types 5 A5S2 Lymphoma2 16 V16E2 Lymphoma2 20 A20T1 Germ cell tumor1 31 K31E Lymphoma2 32 I32V1 Lymphoma1 43 A43*2 Lymphoma2 46 I46*1 T-ALL1, colon carcinoma1 49 R49G1 Lymphoma1 52 T52I1 Mesothelioma1 55 I55*1 Lymphoma ma1 57 C57R2 Lymphoma2 58 R58G1, R58* 1 Germ cell tumor1 64 R64K2 Lymphoma2 77 K77*1 Lymphoma1 80 D80N Lymphoma1 91 Τ9Γ1 Germ cell tumor1 100 T100S1 Lymphoma1 101 D101E2 Lymphoma2 115 K115*1 Lymphoma1 116-126 Mutation splice1 Lymphoma1 116-121 Splice mutation2 Lymphoma2 116-120 Splicing mutation1 Mesothelioma1 133 L133*1 Lymphoma1 134 S134P2 Lymphoma2 137 N137*1 Lymphoma1 143 F143*1 Lymphoma1 152 V152*2 Lymphoma2 165 F165*2 Lymphoma2 167 S167*1 Lymphoma1 168 T168A2 Lymphoma2 170-180 of S170-G1801 Lymphoma1 175- 181 del P175-G1801 Lymphoma1 210 del2101 Lymphoma1 213 G213E Lymphoma2 218 S218F1 Germ cell tumor1 QRFQCn / ZZnZ / q / ΥΙΛΙ 230 V230I2 Lymphoma2 Stop Stop->R Lymphoma2 1Willis, etal. Cell 96.1 (1999):35-45. 2Zhang, et al. Nature Genetics 22.1 (1999): 63-68. As used herein, the term MALT1 protease substrate-associated cancer refers to types of cancer associated with or having a deregulation of a gene, a protein, or the expression, activity or level of any (e.g., one or more) of these associated with a MALT1 protease substrate. In some embodiments, a type of cancer associated with the MALT1 protease substrate is selected from the group consisting of a type of cancer associated with BCL10, a type of cancer associated with A20, a type of cancer associated with CYLD, a type of RelB-associated cancer, regnase-1-associated cancer, roquine-1-associated cancer, HOIL1-associated cancer, NIK-associated cancer, LIMAIa-associated cancer, and combinations of these. In some embodiments, a MALT1 protease substrate-associated cancer type is selected from the group consisting of a BCL10-associated cancer type, an A20-associated cancer type, a CYLD-associated cancer type, and combinations of these. . The types of cancer associated with a particular gene or protein described in this paragraph refer to types of cancer associated with or having a dysregulation of the particular gene, the particular protein, or the expression, activity or level of either ( for example, one or more) of these (for example, any type of deregulation of the particular gene, the particular protein, or the expression, activity or level of any of these described herein). Non-limiting examples of such types of cancer are described herein. Below is an example sequence of human A20: SEQ ID NO: 13 (UniParc Accession No. UPI000000D92D) MAEQVLPQALYLSNMRKAVKIRERTPEDIFKPTNGIIHHFKTMHRYTLEMFRTCQFCPQF REIIHKALIDRNIQATLESQKKLNWCREVRKLVALKTNGDGNCLMHATSQYMWGVQDTDL VLRKALFSTLKETDTRNFKFRWQLESLKSQEFVETGLCYDTRNWNDEWDNLIKMASTDTP MARSGLQYNSLEEIHIFVLCNILR RPIIVISDKMLRSLESGSNFAPLKVGGIYLPLHWPA QECYRYPIVLGYDSHHFVPLVTLKDSGPEIRAVPLVNRDRGRFEDLKVHFLTDPENEMKE KLLKEYLMVIEIPVQGWDHGTTHLINAAKLDEANLPKEINLVDDYFELVQHEYKKWQENS EQGRREGHAQNPMEPSVPQLSLMDVKCETPNCPFFMSVNTQPLCHECSE RRQKNQNKLPK LNSKPGPEGLPGMALGASRGEAYEPLAWNPEESTGGPHSAPPTAPSPFLFSETTAMKCRS PGCPFTLNVQHNGFCERCHNARQLHASHAPDHTRHLDPGKCQACLQDVTRTFNGICSTCF KRTTAEASSSLSTSLPPSCHQRSKSDPSRLVRSPSPHSCHRAGNDAPAGCLSQAARTPGD RTGTSKCRKAGCVYFGTPE NKGFCTLCFIEYRENKHFAAASGKVSPTASRFQNTIPCLGR ECGTLGSTMFEGYCQKCFIEAQNQRFHEAKRTEEQLRSSQRRDVPRTTQSTSRPKFACES CKNILACRSEELCMECQHPNQRMGPGAHRGEPAPEDPPKQRCRAPACDHFGNAKCNGYCN ECFQFKQMYG Non-limiting examples of deregulation of an A20 gene or A20 protein are shown in Table B4 below. Table B4. A20 protein amino acid substitutions / insertions / deletions Amino acid positions Non-limiting example mutations Non-limiting example A20-associated cancer types 100 D100*2 Extranodal marginal zone lymphoma2 162 R162*2 Marginal zone lymph node lymphoma2 183 R183X1 Lymphoma1 271 R271X1 Lymphoma1 278 R278*2 Nodal lymphoma of the marginal zone2 288 V288*2 Splenic lymphoma of the marginal zone2 491 Η49Γ2 Nodal lymphoma of the marginal zone2 633 E633*2 Extranodal lymphoma of the marginal zone2 1Johansson et al. Oncotarget 7.38 (2016): 62627. 2Novak, etal. Blood 113.20 (2009): 4918-4921. QRQQcn / zznz / q / υιλι Below is an example human CYLD sequence: SEQ ID NO: 14 (UniParc Accession No. UPI0000073A15) MSSGLWSQEKVTSPYWEERIFYLLLQECSVTDKQTQKLLKVPKGSIGQYIQDRSVGHSRI PSAKGKKNQIGLKILEQPHAVLFVDEKDWEINEKFTELLLAITNCEERFSLFKNRNRLS KGLQIDVGCPVKVQLRSGEEKFPGWRFRGPLLAERTVSGIFFGVELLEEGRGQGFTDGV YQGKQLFQ CDEDCGVFVALDKLIEDDDTALESDYAGPGDTMQVELPPLEINSRVSLKV GETIESGTVIFCDVLPGKESLGYFVGVDMDNPIGNWDGRFDGVQLCSFACVESTILLHIN DIIPALSESVTQERRPPKLAFMSRGVGDKGSSSHNKPKATGSTSDPGNRNRSELFYTLNG SSVDSQPQSKSKNTWYIDEVAEDPAKSLTEISTDFDRSSP PLQPPPVNSLTTENRFHSLP FSLTKMPNTNGSIGHSPLSLSAQSVMEELNTAPVQESPPLAMPPGNSHGLEVGSLAEVKE NPPFYGVIRWIGQPPGLNEVLAGLELEDECAGCTDGTFRGTRYFTCALKKALFVKLKSCR PDSRFASLQPVSNQIERCNSLAFGGYLSEWEENTPPKMEKEGLEIMIGKKKGIQGHYNS CYLDSTLFCLFAFSS VLDTVLLRPKEKNDVEYYSETQELLRTEIVNPLRIYGYVCATKIM KLRKILEKVEAASGFTSEEKDPEEFLNILFHHILRVEPLLKIRSAGQKVQDCYFYQIFME KNEKVGVPTIQQLLEWSFINSNLKFAEAPSCLIIQMPRFGKDFKLFKKIFPSLELNITDL LEDTPRQCRICGGLAMYECRECYDDPDISAGKIKQFCKTC NTQVHLHPKRLNHKYNPVSL PKDLPDWDWRHGCIPCQNMELFAVLCIETSHYVAFVKYGKDDSAWLFFDSMADRDGGQNG FNIPQVTPCPEVGEYLKMSLEDLHSLDSRRIQGCARRLLCDAYMCMYQSPTMSLYK Non-limiting examples of deregulation of a CYLD gene or a CYLD protein can be found, for example, in Massoumi, Future Oncology 7.2 (2011): 285-297, Alameda, J. P„ etal., Oncogene 29.50 (2010): 6522 -6532, Williams, et al., Modern Pathology (2020): 1-13, and Courtois and Gilmore. Oncogene 25.51 (2006):6831-6843. Below is an example sequence of human RelB: SEQ ID NO: 15 (UniParc Accession No. UPI00000012B7) MLRSGPASGPSVPTGRAMPSRRVARPPAAPELGALGSPDLSSLSLAVSRSTDELEIIDEY IKENGFGLDGGQPGPGEGLPRLVSRGAASLSTVTLGPVAPPATPPPWGCPLGRLVSPAPG PGPQPHLVITEQPKQRGMRFRYECEGRSAGSILGESSTEASKTLPAIELRDCGGLREVEV TACLVWKDWPHRVHPHSLVGKDCTDGICRVRLRPHVSPRHSFNNLGIQCVRKKEIEAAIE RKIQLGIDPYNAGSLKNHQEVDMNWRICFQASYRDQQGQMRRMDPVLSEPVYDKKSTNT SELRICRINKESGPCTGGEELYLLCDKVQKEDISWFSRASWEGRADFSQADVHRQIAIV FKTPPYEDLEIVEPVTVNVFL QRLTDGVCSEPLPFTYLPRDHDSYGVDKKRKRGMPDVLG ELNSSDPHGIESKRRKKKPAILDHFLPNHGSGPFLPPSALLPDPDFFSGTVSLPGLEPPG GPDLLDDGFAYDPTAPTLFTMLDLLPPAPPHASAVVCSGGAGAVVGETPGPEPLTLDSYQ APGPGDGGTASLVGSNMFPNHYREAAFGGGLLSPGPEAT An example sequence of human regnase-1 is shown below: SEQ ID NO: 16 (UniParc Accession No. UPI000004D30E) MSGPCGEKPVLEASPTMSLWEFEDSHSRQGTPRPGQELAAEEASALELQMKVDFFRKLGY SSTEIHSVLQKLGVQADTNTVLGELVKHGTATERERQTSPDPCPQLPLVPRGGGTPKAPN LEPPLPEEEKEGSDLRPWIDGSNVAMSHGNKEVFSCRGILLAVNWFLERGHTDITVFVP SWRKEQPRPDVPITDQHILRELEKKKILVFTPSRRVGGKRWCYDDRFIVKLAYESDGIV VSNDTYRDLQGERQEWKRFIEERLLMYSFVNDKFMPPDDPLGRHGPSLDNFLRKKPLTLE HRKQPCPYGRKCTYGIKCRFFHPERPSCPQRSVADELRANALLSPPRAPSKDKNGRRPSP SSQSSSLLTESEQCSLDGKKLGAQASPGSRQEGLTQTYAPSGRSLAPSGGSGSSFGPTDW LPQTLDSLPYVSQDCLDSGIGSLESQMSELWGVRGGGPGEPGPPRAPYTGYSPYGSELPA TAAFSAFGRAMGAGHFSVPADYPPAPPAFPPREYWSEPYPLPPPTSVLQEPPVQSPGAGR SPWGRAGSLAKEQASVYTKLCGVFPPHLVEAVMGRFPQLLDPQQLAAEILSYKSQHPSE Below is an example sequence of human roquina-1: SEQ ID NO: 17 (UniParc Accession No. UPI00001D7DA8) MPVQAPQWTDFLSCPICTQTFDETIRKPISLGCGHTVCKMCLNKLHRKACPFDQTTINTD IELLPVNSALLQLVGAQVPEQQPITLCSGVEDTKHYEEAKKCVEELALYLKPLSSARGVG LNSTTQSVLSRPMQRKLVTLVHCQLVEEEGRIRAMRAARSLGERTVTELILQHQNPQQLS SNLWAAVRARGCQFLGPAMQEEALKLVLLALEDGSALSRKVLVLFWQRLEPRFPQASKT SIGHWQLLYRASCFKVTKRDEDSSLMQLKEEFRTYEALRREHDSQIVQIAMEAGLRIAP DQWSSLLYGDQSHKSHMQSIIDKLQTPASFAQSVQELTIALQRTGDPANLNRLRPHLELL ANIDPSPDAPPPTWEQLENGLVAVRTWHGLVDYIQNHSKKGADQQQPPQHSKYKTYMCR DMKQRGGCPRGASCTFAHSQEELEKFRKMNKRLVPRRPLSASLGQLNEVGLPSAAILPDE GAVDLPSRKPPALPNGIVSTGNTVTQLIPRGTDPSYDSSLKPGKIDHLSSSAPGSPPDLL ESVPKSISALPVNPHSIPRGPADLPPMPVT KPLQMVPRGSQLYPAQQTDVYYQDPRGAA PPFEPAPYQQGMYYTPPPQCVSRFVRPPPSAPEPAPPYLDHYPPYLQERWNSQYGTQPQ QYPPIYPSHYDGRRVYPAPSYTREEIFRESPIPIEIPPAAVPSYVPESRERYQQIESYYP VAPHPTQIRPSYLREPPYSRLPPPPQPHPSLDELHRRRKEIMAQ READKVISPPPFAPSP TLPPTFHPEEFLDEDLKVAGKYKGNDYSQYSPWSCDTIGSYIGTKDAKPKDWAAGSVEM MNVESKGMRDQRLDLQRRAAETSDDDLIPFGDRPTVSRFGAISRTSKTIYQGAGPMQAMA PQGAPTKSINISDYSPYGTHGGWGASPYSPHQNIPSQGHFSERERISMSEVASHGKPLPS AERE QLRLELQQLNHQISQQTQLRGLEAVSNRLVLQREANTLAGQSQPPPPPPPPKWPGMI SSEQLSLELHQVEREIGKRTRELSMENQCSLDMKSKLNTSKQAENGQPEPQNKVPAEDLT LTFSDVPNGSALTQENISLLSNKTSSLNLSEDPEGGGDNNDSQRSGVTPSSAP Below is an example sequence of human HOIL1: SEQ ID NO: 17 (UniParc Accession No. UPI000006F045) MDEKTKKAEEMALSLTRAVAGGDEQVAMKCAIWLAEQRVPLSVQLKPEVSPTQDIRLWVS VEDAQMHTVTIWLTVRPDMTVASLKDMVFLDYGFPPVLQQWVIGQRLARDQETLHSHGVR QNGDSAYLYLLSARNTSLNPQELQRERQLRMLEDLGFKDLTLQPRGPLEPGPPKPGVPQE PGRGQPDAVPEPPPVGW QCPGCTFINKPTRPGCEMCCRARPEAYQVPASYQPDEEERARL AGEEEALRQYQQRKQQQQEGNYLQHVQLDQRSLVLNTEPAECPVCYSVLAPGEAWLREC LHTFCRECLQGTIRNSQEAEVSCPFIDNTYSCSGKLLEREIKALLTPEDYQRFLDLGISI AENRSAFSYHCKTPDCKGWCFFEDDVNEFTCPVCFHVNCLLC KAIHEQMNCKEYQEDLAL RAQNDVAARQTTEMLKVMLQQGEAMRCPQCQIWQKKDGCDWIRCTVCHTEICWVTKGPR WGPGGPGDTSGGCRCRVNGIPCHPSCQNCH Below is an example human NIK sequence: SEQ ID NO: 18 (UniParc Accession No. UPI0000074220) MAVMEMACPGAPGSAVGQQKELPKAKEKTPPLGKKQSSVYKLEAVEKSPVFCGKWEILND VITKGTAKEGSEAGPAAISIIAQAECENSQEFSPTFSERIFIAGSKQYSQSESLDQIPNN VAHATEGKMARVCWKGKRRSKARKKRKKKSSKSLAHAGVALAKPLPRTPEQESCTIPVQE DESPLGAPYVRNTPQFTKPLKEPGLG QLCFKQLGEGLRPALPRSELHKLISPLQCLNHVW KLHHPQDGGPLPLPTHPFPYSRLPHPFPFHPLQPWKPHPLESFLGKLACVDSQKPLPDPH LSKLACVDSPKPLPGPHLEPSCLSRGAHEKFSVEEYLVHALQGSVSSGQAHSLTSLAKTW AARGSRSREPSPKTEDNEGVLLTEKLKPVDYEYREEVHWATHQLRLGRGSF GEVHRMEDK QTGFQCAVKKVRLEVFRAEELMACAGLTSPRIVPLYGAVREGPWVNIFMELLEGGSLGQL VKEQGCLPEDRALYYLGQALEGLEYLHSRRILHGDVKADNVLLSSDGSHAALCDFGHAVC LQPDGLGKSLLTGDYIPGTETHMAPEWLGRSCDAKVDVWSSCCMMLHMLNGCHPWTQFF RGPLCLKIASEPPPVREIPPSCAPLTAQAIQEGLRKEPIHRVSAAELGGKVNRALQQVGG LKSPWRGEYKEPRHPPPNQANYHQTLHAQPRELSPRAPGPRPAEETTGRAPKLQPPLPPE PPEPNKSPPLTLSKEESGMWEPLPLSS LEPAPARNPSSPERKATVPEQELQQLEIELFLN SLSQPFSLEEQEQILSCLSIDSLSLSDDSEKNPSKASQSSRDTLSSGVHSWSSQAEARSS SWNMVLARGRPTDTPSYFNGVKVQIQSLNGEHLHIREFHRVKVGDIATGISSQIPAAAFS LVTKDGQPVRYDMEVPDSGIDLQCTLAPDGSFAWSWRVKHGQLENRP Below is an example sequence of human LIMAIa: SEQ ID NO: 19 (UniParc Accession No. UPI000002A906) MENCLGESRHEVEKSEISENTDASGKIEKYNVPLNRLKMMFEKGEPTQTKILRAQSRSAS GRKISENSYSLDDLEIGPGQLSSSTFDSEKNESRRNLELPRLSETSIKDRMAKYQAAVSK QSSSTNYTNELKASGGEIKIHKMEQKENVPPGPEVCITHQEGEKISANENSLAVRSTPAE DDSRDSQVKSEVQQPVHPKPLSPDSRASSLSESSPPKAMKKFQAPARETCVECQKTVYPM ERLLANQQVFHISCFRCSYCNNKLSLG TYASLHGRIYCKPHFNQLFKSKGNYDEGFGHRP HKDLWASKNENEEILERPAQLANARETPHSPGVEDAPIAKVGVLAASMEAKASSQQEKED KPAETKKLRIAWPPPTELGSSGSALEEGIKMSKPKWPPEDEISKPEVPEDVDLDLKKLRR SSSLKERSRPFTVAASFQSTSVKSPKTVSPPIRKGWSMSEQSEESVGGR VAERKQVENAK ASKKNGNVGKTTWQNKESKGETGKRSKEGHSLEMENENLVENGADSDEDDNSFLKQQSPQ EPKSLNWSSFVDNTFAEEFTTQNQKSQDVELWEGEWKELSVEEQIKRNRYYDEDEDEE As used herein, the term cancer associated with a component of the NF-κΒ pathway downstream of a CBM complex refers to types of cancer associated with or having a deregulation of a gene, protein, or expression, activity or level of any (e.g., one or more) of these associated with a component of the NFkB pathway downstream of a CBM complex. In some embodiments, a cancer type associated with a component of the NF-κΒ pathway downstream of a CBM complex is selected from the group consisting of a TAK1-associated cancer, a TRAF6-associated cancer, a type of cancer associated with TAB1, type of cancer associated with TAB2, type of cancer associated with TAB3, type of cancer associated with MKK7, type of cancer associated with IKKa, type of cancer associated with ΙΚΚβ, type of IKKy-associated cancer, an IkBa-associated cancer, a p50-associated cancer, a p65 (RelA)-associated cancer, a c-Rel-associated cancer, and combinations thereof. In some embodiments, a cancer associated with a component of the NF-κΒ pathway downstream of a CBM complex is an IKKy-associated cancer. The types of cancer associated with a particular gene or protein described in this paragraph refer to types of cancer associated with or having a dysregulation of the particular gene, the particular protein, or the expression, activity or level of either ( for example, one or more) of these (for example, any type of deregulation of the particular gene, the particular protein, or the expression, activity or level of any of these described herein). Non-limiting examples of such types of cancer are described herein. Below is an example sequence of human TAK1: SEQ ID NO: 20 (UniParc Accession No. UPI000012EAD6) MSTASAASSSSSSSAGEMIEAPSQVLNFEEIDYKEIEVEEWGRGAFGWCKAKWRAKDV AIKQIESESERKAFIVELRQLSRVNHPNIVKLYGACLNPVCLVMEYAEGGSLYNVLHGAE PLPYYTAAHAMSWCLQCSQGVAYLHSMQPKALIHRDLKPPNLLLVAGGTVLKICDFGTAC DIQTHMTNNKGSAAWMAPEVFEGSNYSEKCDVFSWGIILWEVITRRKPFDEIGGPAFRIM WAVHNGTRPPLIKNLPKPIESLMTRC WSKDPSQRPSMEEIVKIMTHLMRYFPGADEPLQY PCQYSDEGQSNSATSTGSFMDIASTNTSNKSDTNMEQVPATNDTIKRLESKLLKNQAKQQ SESGRLSLGASRGSSVESLPPTSEGKRMSADMSEIEARIAATTAYSKPKRGHRKTASFGN ILDVPEIVISGNGQPRRRSIQDLTVTGTEPGQVSSRSSSPSVRMITTSGPTSEKPTRSHP W TPDDSTDTNGSDNSIPMAYLTLDHQLQPLAPCPNSKESMAVFEQHCKMAQEYMKVQTEI ALLLQRKQELVAELDQDEKDQQNTSRLVQEHKKLLDENKSLSTYYQQCKKQLEVIRSQQQ KRQGTS Below is an example sequence of human TRAF6: SEQ ID NO: 21 (UniParc Accession No. UPI000000D924) MSLLNCENSCGSSQSESDCCVAMASSCSAVTKDDSVGGTASTGNLSSSFMEEIQGYDVEF DPPLESKYECPICLMALREAVQTPCGHRFCKACIIKSIRDAGHKCPVDNEILLENQLFPD NFAKREILSLMVKCPNEGCLHKMELRHLEDHQAHCEFALMDCPQCQRPFQKFHINIHILK DCPRRQVSCDNCAASMAFEDKEIHDQNCPLANVICEYCNTILIREQMPNHYDLDCPTAPI PCTFSTFGCHEKMQRNHLARHLQENTQ SHMRMLAQAVHSLSVIPDSGYISEVRNFQETIH QLEGRLVRQDHQIRELTAKMETQSMYVSELKRTIRTLEDKVAEIEAQQCNGIYIWKIGNF GMHLKCQEEEKPWIHSPGFYTGKPGYKLCMRLHLQLPTAQRCANYISLFVHTMQGEYDS HLPWPFQGTIRLTILDQSEAPVRQNHEEIMDAKPELLAFQRPTI PRNPKGFGYVTFMHLE ALRQRTFIKDDTLLVRCEVSTRFDMGSLRREGFQPRSTDAGV Below is an example sequence of human TAB1: SEQ ID NO: 22 (UniParc Accession No. UPI0000136861) MAAQRRSLLQSEQQPSWTDDLPLCHLSGVGSASNRSYSADGKGTESHPPEDSWLKFRSEN NCFLYGVFNGYDGNRVTNFVAQRLSAELLLGQLNAEHAEADVRRVLLQAFDWERSFLES IDDALAEKASLQSQLPEGVPQHQLPPQYQKILERLKTLEREISGGAMAWAVLLNNKLYV ANVGTNRALLCKSTVDGLQVTQ LNVDHTTENEDELFRLSQLGLDAGKIKQVGIICGQEST RRIGDYKVKYGYTDIDLLSAAKSKPIIAEPEIHGAQPLDGVTGFLVLMSEGLYKALEAAH GPGQANQEIAAMIDTEFAKQTSLDAVAQAWDRVKRIHSDTFASGGERARFCPRHEDMTL LVRNFGYPLGEMSQPTPSPAPAAGGRVYPVSVPYSSAQSTSKTSVTLS LVMPSQGQMVNG AHSASTLDEATPTLTNQSPTLTLQSTNTHTQSSSSSSDGGLFRSRPAHSLPPGEDGRVEP YVDFAEFYRLWSVDHGEQSWTAP Below is an example sequence of human TAB2: QRFQCn / ZZnZ / q / ΥΙΛΙ SEQ ID NO: 23 (UniParc Accession No. UPI0000073C75) MAQGSHQIDFQVLHDLRQKFPEVPEVVVSRCMLQNNNNLDACCAVLSQESTRYLYGEGDL NFSDDSGISGLRNHMTSLNLDLQSQNIYHHGREGSRMNGSRTLTHSISDGQLQGGQSNSE LFQQEPQTAPAQVPQGFNVFGMSSSSGASNSAPHLGFHLGSKGTSSLSQQTPRFNPIMVT LAPNIQTGRNTPTSLHIHGV PPPVLNSPQGNSIYIRPYITTPGGTTRQTQQHSGWVSQFN PMNPQQVYQPSQPGPWTTCPASNPLSHTSSQQPNQQGHQTSHVYMPISSPTTSQPPTIHS SGSSQSSAHSQYNIQNISTGPRKNQIEIKLEPPQRNNSSKLRSSGPRTSSTSSSVNSQTL NRNQPTVYIAASPPNTDELMSRSQPKVY ISANAATGDEQVMRNQPTLFISTNSGASAASR NMSGQVSMGPAFIHHHPPKSRAIGNNSATSPRWVTQPNTKYTFKITVSPNKPPAVSPGV VSPTFELTNLLNHPDHYVETENIQHLTDPTLAHVDRISETRKLSMGSDDAAYTQALLVHQ KARMERLQRELEIQKKKLDKLKSEVNEMENNLTRRRLKRSNSISQIPSLEEMQQLRSCNR QL QIDIDCLTKEIDLFQARGPHFNPSAIHNFYDNIGFVGPVPPKPKDQRSIIKTPKTQDT EDDEGAQWNCTACTFLNHPALIRCEQCEMPRHF Below is an example sequence of human TAB3: SEQ ID NO: 24 (UniParc Accession No. UPI0000071648) MAQSSPQLDIQVLHDLRQRFPEIPEGWSQCMLQNNNNLEACCRALSQESSKYLYMEYHS PDDNRMNRNRLLHINLGIHSPSSYHPGDGAQLNGGRTLVHSSSDGHIDPQHAAGKQLICL VQEPHSAPAWAATPNYNPFFMNEQNRSAATPPSQPPQQPSSMQTGMNPSAMQGPSPPPP PPSYMHIPRYSTNPITVTVSQNLPS GQTVPRALQILPQIPSNLYGSPGSIYIRQTSQSSS GRQTPQSTPWQSSPQGPVPHYSQRPLPVYPHQQNYQPSQYSPKQQQIPQSAYHSPPPSQC PSPFSSPQHQVQPSQLGHIFMPPSPSTTPPHPYQQGPPSYQKQGSHSVAYLPYTASSLSK GSMKKIEITVEPSQRPGTAINRSPSPISNQPSPRNQHSLY TATTPPSSSPSRGISSQPKP PFSVNPVYITYTQPTGPSCTPSPSPRVIPNPTTVFKITVGRATTENLLNLVDQEERSAAP EPIQPISVIPGSGGEKGSHKYQRSSSSGSDDYAYTQALLLHQRARMERLAKQLKLEKEEL ERLKSEVNGMEHDLMQRRLRRVSCTTAIPTPEEMTRLRSMNRQLQINVDCTLKEVDLLQS RGNFDPKAMNNFYDNIEPGPWPPKPSKKDSSDPCTIERKARRISVTSKVQADIHDTQAA AADEHRTGSTQSPRTQPRDEDYEGAPWNCDSCTFLNHPALNRCEQCEMPRYT Below is an example sequence of human MKK7: SEQ ID NO: 25 (UniParc Accession No. UPI000012F494) MAASSLEQKLSRLEAKLKQENREARRRIDLNLDISPQRPRPTLQLPLANDGGSRSPSSES SPQHPTPPARPRHMLGLPSTLFTPRSMESIEIDQKLQEIMKQTGYLTIGGQRYQAEINDL ENLGEMGSGTCGQVWKMRFRKTGHVIAVKQMRRSGNKEENKRILMDLDWLKSHDCPYIV QCFGTFITNTDVFIAMELMGTCAEKLKKRMQGPI PERILGKMTVAIVKALYYLKEKHGVI HRDVKPSNILLDERGQIKLCDFGISGRLVDSKAKTRSAGCAAYMAPERIDPPDPTKPDYD IRADVWSLGISLVELATGQFPYKNCKTDFEVLTKVLQEEPPLLPGHMGFSGDFQSFVKDC QRQQcn / zznz / q / υιλι LTKDHRKRPKYNKLLEHSFIKRYETLEVDVASWFKDVMAKTESPRTSGVLSQPHLPFFR Below is an example human IKKo sequence: SEQ ID NO: 26 (UniParc Accession No. UPI000013D6C7) MERPPGLRPGAGGPWEMRERLGTGGFGNVCLYQHRELDLKIAIKSCRLELSTKNRERWCH EIQIMKKLNHANWKACDVPEELNILIHDVPLLAMEYCSGGDLRKLLNKPENCCGLKESQ ILSLLSDIGSGIRYLHENKIIHRDLKPENIVLQDVGGKIIHKIIDLGYAKDVDQGSLCTS FVGTLQYLAPELFENKPYTATVDYWSFGTMVF ECIAGYRPFLHHLQPFTWHEKIKKKDPK CIFACEEMSGEVRFSSHLPQPNSLCSLVVEPMENWLQLMLNWDPQQRGGPVDLTLKQPRC FVLMDHILNLKIVHILNMTSAKIISFLLPPDESLHSLQSRIERETGINTGSQELLSETGI SLDPRKPASQCVLDGVRGCDSYMVYLFDKSKTVYEGPFASRSLSDCVNYIVQDSKIQLPI I QLRKVWAEAVHYVSGLKEDYSRLFQGQRAAMLSLLRYNANLTKMKNTLISASQQLKAKL EFFHKSIQLDLERYSEQMTYGISSEKMLKAWKEMEEKAIHYAEVGVIGYLEDQIMSLHAE IMELQKSPYGRRQGDLMESLEQRAIDLYKQLKHRPSDHSYSDSTEMVKIIVHTVQSQDRV LKELFGHLSK LLGCKQKIIDLLPKVEVALSNIKEADNTVMFMQGKRQKEIWHLLKIACTQ SSARSLVGSSLEGAVTPQTSAWLPPTSAEHDHSLSCVVTPQDGETSAQMIEENLNCLGHL STIIHEANEEQGNSMMNLDWSWLTE Below is an example sequence of human IΚΚβ: SEQ ID NO: 27 (UniParc Accession No. UPI0000033729) MSWSPSLTTQTCGAWEMKERLGTGGFGNVIRWHNQETGEQIAIKQCRQELSPRNRERWCL EIQIMRRLTHPNVVAARDVPEGMQNLAPNDLPLLAMEYCQGGDLRKYLNQFENCCGLREG AILTLLSDIASALRYLHENRIIHRDLKPENIVLQQGEQRLIHKIIDLGYAKELDQGSLCT SFVGTLQYLAPELLEQQKYTV TVDYWSFGTLAFECITGFRPFLPNWQPVQWHSKVRQKSE VDIWSEDLNGTVKFSSSLPYPNNLNSVLAERLEKWLQLMLMWHPRQRGTDPTYGPNGCF KALDDILNLKLVHILNMVTGTIHTYPVTEDESLQSLKARIQQDTGIPEEDQELLQEAGLA LIPDKPATQCISDGKLNEGHTLDMDLLVFLFDNSKITYETQISPRPQPESVSC ILQEPKRN LAFFQLRKVWGQVWHSIQTLKEDCNRLQQGQRAAMMNLLRNNSCLSKMKNSMASMSQQLK AKLDFFKTSIQIDLEKYSEQTEFGITSDKLLLAWREMEQAVELCGRENEVKLLVERMMAL QTDIVDLQRSPMGRKQGGTLDDLEEQARELYRRLREKPRDQRTEGDSQEMVRLLLQAIQS FEKKVRVIYT QLSKTWCKQKALELLPKVEEWSLMNEDEKTWRLQEKRQKELWNLLKI ACSKVRGPVSGSPDSMNASRLSQPGQLMSQPSTASNSLPEPAKKSEELVAEAHNLCTLLE NAIQDTVREQDQSFTALDWSWLQTEEEEHSCLEQAS Below is an example sequence of human ΙΚΚγ: SEQ ID NO: 28 (UniParc Accession No. UPI0000000CC4) MNRHLWKSQLCEMVQPSGGPAADQDVLGEESPLGKPAMLHLPSEQGAPETLQRCLEENQE LRDAIRQSNQILRERCEELLHFQASQREEKEFLMCKFQEARKLVERLGLEKLDLKRQKEQ ALREVEHLKRCQQQMAEDKASVKAQVTSLLGELQESQSRLEAATKECQALEGRARAASEQ ARQLESEREALQQQHSVQVDQLRMQGQSVEAALRMERQAASEEKRKLAQLQVAYHQLFQE YDNHIKSSWGSERKRGMQLEDLKQQLQQAEEALVAKQEVIDKLKEEAEQHKIVMETVPV LKAQADIYKADFQAERQAREKLAEKKELLQEQLEQLQREYSKLKASCQESARIEDMRKRH VEVSQAPLPPAPAYLSSPLALPSQRRSPPEEPPDFCCPKCQYQAPDMDTLQIHVMECIE Non-limiting examples of deregulation of a ΙΚΚγ gene or a ΙΚΚγ protein are described, for example, in Courtois and Gilmore, Oncogene 25.51 (2006): 6831-6843. Below is an example sequence of human IkBa: SEQ ID NO: 29 (UniParc Accession No. UPI000004F0A9) MFQAAERPQEWAMEGPRDGLKKERLLDDRHDSGLDSMKDEEYEQMVKELQEIRLEPQEVP RGSEPWKQQLTEDGDSFLHLAIIHEEKALTMEVIRQVKGDLAFLNFQNNLQQTPLHLAVI TNQPEIAEALLGAGCDPELRDFRGNTPLHLACEQGCLASVGVLTQSCTTPHLHSILKATN YNGHTCLHLASIHGYLGIVELLVSLGADVNAQEPCNGRTALHLAVDLQNPDLVSLLLKCG ADVNRVTYQGYSPYQLTWGRPSTRIQQQLGQLTLENLQMLPESEDEESYDTESEFTEFTE DELPYDDCVFGGQRLTL Below is an example sequence of human p105, which is processed into p50: SEQ ID NO: 30 (UniParc Accession No. UPI000000D917) MAEDDPYLGRPEQMFHLDPSLTHTIFNPEVFQPQMALPTDGPYLQILEQPKQRGFRFRYV CEGPSHGGLPGASSEKNKKSYPQVKICNYVGPAKVIVQLVTNGKNIHLHAHSLVGKHCED GICTVTAGPKDMWGFANLGILHVTKKKVFETLEARMTEACIRGYNPGLLVHPDLAYLQA EGGGDRQLGDREKELIRQAALQQTKEMDLSWRLMFTAFLPDSTGSFTRRLEPWSDAIY DSKAPNASNLKIVRMDRTAGCVTGGEEIYLLCDKVQKDDIQIRFYEEEENGGVWEGFGDF SPTDVHRQFAIVFKTPKYKDINITKPASVFVQLRRKSDLETSEPKPFLYYPEIKDKEEVQ RKRQKLMPNFSDSFGGGSGAGAGGGGMFGSGGGGGGTGSTGPGYSFPHYGFPTYGGITFH PGTTKSNAGMKHGTMDTESKKDPEGCDKSDDKNTVNLFGKVIETTEQDQEPSEATVGNGE VTLTYATGTKEESAGVQDNLFLEKAMQLAKRHANALFDYAVTGDVKMLLAVQRHLTAVQD ENGDSVLHLAIIHLHSQLVRDLLEVTSGLISDDIINMRNDLYQTPLHLAVITKQEDWED LLRAGADLSLLDRLGNSVLHLAAKEGHDKVLSILLKHKKAALLLDHPNGDGLNAIHLAMM SNSLPCLLLLVAAGADVNAQEQKSGRTALHLAVEHDNISLAGCLLLEGDAHVDSTTYDGT TPLHIAAGRGSTRLAALLKAAGADPLVENFEPLYDLDDSWENAGEDEGWPGTTPLDMAT SWQVFDILNGKPYEPEFTSDDLLAQGDMKQLAEDVKLQLYKLLEIPDPDKNWATLAQKLG LGILNNAFRLSPAPSKTLMDNYEVSGGTVRELVEALRQMGYTEAIEVIQAASSPVKTTSQ AHSLPLSPASTRQQIDELRDSDSVCDSGVETSFRKLSFTESLTSGASLLTLNKMPHDYGQ EGPLEGKI Below is an example sequence of human p65: SEQ ID NO: 31 (UniParc Accession No. UPI000013ED68) MDELFPLIFPAEPAQASGPYVEIIEQPKQRGMRFRYKCEGRSAGSIPGERSTDTTKTHPT IKINGYTGPGTVRISLVTKDPPHRPPHHELVGKDCRDGFYEAELCPDRCIHSFQNLGIQC VKKRDLEQAISQRIQTNNNPFQVPIEEQRGDYDLNAVRLCFQVTVRDPSGRPLRLPPVLS HPIFDNRAPNTAELKICRVNRNSGSCLGGDE IFLLCDKVQKEDIEVYFTGPGWEARGSFS QADVHRQVAIVFRTPPYADPSLQAPVRVSMQLRRPSDRELSEPMEFQYLPDTDDRHRIEE KRKRTYETFKSIMKKSPFSGPTDPRPPPRRIAVPSRSSASVPKPAPQPYPFTSSLSTINY DEFPTMVFPSGQISQASALAPAPPQVLPQAPAPAPAPAMVSALAQAPAPVPVLA PGPPQA VAPPAPKPTQAGEGTLSEALLQLQFDDEDLGALLGNSTDPAVFTDLASVDNSEFQQLLNQ GIPVAPHTTEPMLMEYPEAITRLVTGAQRPPDPAPAPLGAPGLPNGLLSGDEDFSSIADM DFSALLSQISS Below is an example human c-Rel sequence: SEQ ID NO: 32 (UniParc Accession No. UPI000013367B) MASGAYNPYIEIIEQPRQRGMRFRYKCEGRSAGSIPGEHSTDNNRTYPSIQIMNYYGKGK VRITLVTKNDPYKPHPHDLVGKDCRDGYYEAEFGQERRPLFFQNLGIRCVKKKEVKEAII TRIKAGINPFNVPEKQLNDIEDCDLNWRLCFQVFLPDEHGNLTTALPPWSNPIYDNRA PNTAELRICRVNKNCGSVRGGDEIFLLCDKVQKDDIEVRFVLNDWEAKGIFSQADVHRQV AIVFKTPPYCKAITEPVTVK MQLRRPSDQEVSESMDFRYLPDEKDTYGNKAKKQKTTLLF QKLCQDHVETGFRHVDQDGLELLTSGDPPTLASQSAGITVNFPERPRPGLLGSIGEGRYF KKEPNLFSHDAVVREMPTGVSSQAESYYPSPGPISSGLSHHASMAPLPSSSWSSVAHPTP RSGNTNPLSSFSTRTLPSNSQGIPPFLRIPVGNDLNASNACIYNNADDIVGMEASSMPSA DLYGI SDPNMLSNCSVNMMTTSDSMGETDNPRLLSMNLENPSCNSVLDPRDLRQLHQMS SSSMSAGANSNTTVFVSQSDAFEGSDFSCADNSMINESGPSNSTNPNSHGFVQDSQYSGI GSMQNEQLSDSFPYEFFQV As used herein, the term cancer associated with a component of the JNK pathway downstream of a CBM complex refers to types of cancer associated with or having a deregulation of a gene, a protein, or in the expression, activity or level of any (e.g., one or more) of these associated with a component of the JNK pathway downstream of a CBM complex. In some embodiments, a type of cancer associated with a component of the JNK pathway downstream of a CBM complex is selected from the group consisting of a type of cancer associated with JNK1, a type of cancer associated with JNK2, a type of JNK3-associated cancer, a MYD88 transcription factor-associated cancer, an AP-1 transcription factor-associated cancer, and combinations thereof. The types of cancer associated with a particular gene or protein described in this paragraph refer to types of cancer associated with or having a deregulation of the particular gene, the particular protein, or in the expression, activity or level of any (e.g., one or more) of these (e.g., any of the types of gene deregulation in QRFQCn / ZZnZ / q / ΥΙΛΙ, the particular protein, or in the expression, activity or level of any of these described herein). Non-limiting examples of such types of cancer are described herein. Below is an example sequence of human JNK1: SEQ ID NO: 33 (UniParc Accession No. UPI000012F17A) MSRSKRDNNFYSVEIGDSTFTVLKRYQNLKPIGSGAQGIVCAAYDAILERNVAIKKLSRP FQNQTHAKRAYRELVLMKCVNHKNIIGLLNVFTPQKSLEEFQDVYIVMELMDANLCQVIQ MELDHERMSYLLYQMLCGIKHLHSAGIIHRDLKPSNIVVKSDCTLKILDFGLARTAGTSF MMTPYWTRYYRAPEVILGMGYKENVDLWSVGCIMGEMVCHKILFPGRDYIDQWNKVIEQ LGTPCPEFMKKLQPTVRTYVENRPKYAGYSFEKLFPDVLFPADSEHNKLKASQARDLLSK MLVIDASKRISVDEALQHPYINVWYDPSEAEAPPPKIPDKQLDEREHTIEEWKELIYKEV MDLEERTKNGVIRGQPSPLGAAVINGSQHPSSSSSVNDVSSMSTDPTLASDTDSSLEAAA GPLGCCR Below is an example sequence of human JNK2: SEQ ID NO: 34 (UniParc Accession No. UPI000006E3AD) MSDSKCDSQFYSVQVADSTFTVLKRYQQLKPIGSGAQGIVCAAFDTVLGINVAVKKLSRP FQNQTHAKRAYRELVLLKCVNHKNIISLLNVFTPQKTLEEFQDVYLVMELMDANLCQVIH MELDHERMSYLLYQMLCGIKHLHSAGIIHRDLKPSNIVVKSDCTLKILDFGLARTACTNF MMTPYWTRYYRAPEVILGMGYKENVDIWSVGCIMGELVKGCVIFQGTDHIDQWNKVIEQ LGTPSAEFMKKLQPTVRNYVENRPKYPGIKFEELFPDWIFPSESERDKIKTSQARDLLSK MLVIDPDKRISVDEALRHPYITVWYDPAEAEAPPPQIYDAQLEEREHAIEEWKELIYKEV MDWEERSKNGWKDQPSDAAVSSNATPSQSSSINDISSMSTEQTLASDTDSSLDASTGPL EGCR Below is an example sequence of human JNK3: SEQ ID NO: 35 (UniParc Accession No. UPI0000049042) MSLHFLYYCSEPTLDVKIAFCQGFDKQVDVSYIAKHYNMSKSKVDNQFYSVEVGDSTFTV LKRYQNLKPIGSGAQGIVCAAYDAVLDRNVAIKKLSRPFQNQTHAKRAYRELVLMKCVNH KNIISLLNVFTPQKTLEEFQDVYLVMELMDANLCQVIQMELDHERMSYLLYQMLCGIKHL HSAGIIHRDLKPSNIWKSDCTLKILDFGLARTAGTSFMMTPYWTRYYRAPEVILGMGY KENVDIWSVGCIMGEMVRHKILFPGRDYIDQWNKVIEQLGTPCPEFMKKLQPTVRNYVEN RPKYAGLTFPKLFPDSLFPADSEHNKLKASQARDLLSKMLVIDPAKRISVDDALQHPYIN VWYDPAEVEAPPPQIYDKQLDEREHTIEEWKELIYKEVMNSEEKTKNGWKGQPSPSGAA VNSSESLPPSSSVNDISSMSTDQTLASDTDSSLEASAGPLGCCR Compounds of Formula (I) Provided herein are compounds of Formula (I), or a pharmaceutically acceptable salt thereof: R2 where: each is a single or double bond; XesNoC; YesNoC; ZesNoCR5; where, when one of X and Y is N, the other of X and Y is C; n is 1,2 or 3; R1 is hydrogen, halogen, cyano, hydroxyl, C1-C3 alkoxy, C1-C3 haloalkoxy, C1-C3 haloalkyl, -NRARBo C1-C3 alkyl optionally substituted with 1-3 substituents independently selected from hydroxyl and C1-C3 alkoxy; R2 is hydrogen, amino or halogen; R2A is hydrogen, halogen or C1-C6 alkyl; each R3 is independently halogen, hydroxyl, cyano, C3-C6 cycloalkyl, -NRARB, 5-6 membered heteroaryl optionally substituted with C1-C3 alkyl; C1-C3 alkoxy, C1-C3 haloalkoxy, C1-C3 haloalkyl or C1-C3 alkyl optionally substituted with a C1-C3 alkoxy or cyano; or two R3, together with the carbon atom to which they are attached, join together to form an oxo group or a C3-C8 cycloalkyl; m is 0,1,2 or 3; R4 is phenyl, naphthyl, 5-10 membered heteroaryl, 3-10 membered heterocyclyl or C3-C8 cycloalkyl; wherein each R4 group is optionally substituted with 1-3 substituents independently selected from R6; R5 is hydrogen, halogen, cyano, hydroxyl, C1-C3 alkoxy, C1-C3 haloalkoxy, C1-C3 haloalkyl, -NRCRDo C1-C3 alkyl; and each R6 is independently selected from halogen; cyan; hydroxyl; -CO2H; -N=(S=O)(C1 -C3 alkyl)?, -S(=O)P(C1C3 alkyl), -NRERF; -(C=O)NRERF; C1-C3 alkoxy optionally substituted with amino, hydroxyl or -(C=O)NRERF; C1-C3 haloalkyl; C1-C3 haloalkoxy; 5-6 membered heteroaryl optionally substituted with 1-3 independently selected Rx; C1-C3 alkyl optionally substituted with 1-2 substituents independently selected from hydroxyl, -NRERF, C1-C3 alkoxy and C3-C6 cycloalkyl; C3-C6 cycloalkyl optionally substituted with hydroxyl; and —(Q)q3-8 membered heterocyclyl optionally substituted with independently selected 1-3 C1-C3 alkyl; p is 1 or 2; Qes -O-O-NH-; q is 0 or 1; each Rx is independently selected from halogen, cyano, hydroxyl, amino, C1-C3 alkoxy, C1-C3 haloalkoxy, C1-C3 haloalkyl or C1-C6 alkyl optionally substituted with 1-3 substituents independently selected from hydroxyl, C1-C3 alkoxy and - NRGRH; and RA, RB, Rc, RD are independently hydrogen, C1-C3 alkyl, or RA, and RB, or Rcy RD, together with the nitrogen atom to which they are attached, join to form a 4-6 membered heterocyclyl; and RE, RF, RGy RH are independently hydrogen, C1-C3 alkyl or C3-C6 cycloalkyl, or REy RF, or RGy RH, together with the nitrogen atom to which they are attached, join to form a 4-6 membered heterocyclyl optionally substituted with C1-C3 alkyl or C1-C3 alkoxy. In some modalities: each is a single or double bond; XesNoC; YesNoC; Z is N or CR5; where, when one of X and Y is N, the other of X and Y is C; n is 1,2 or 3; R1 is hydrogen, halogen, cyano, hydroxyl, C1-C3 alkoxy, C1-C3 haloalkoxy, C1-C3 haloalkyl, -NRARBo C1-C3 alkyl optionally substituted with 1-3 substituents independently selected from hydroxyl and C1-C3 alkoxy; R2 is hydrogen or halogen; R2A is hydrogen; each R3 is independently halogen, hydroxyl, C3-C6 cycloalkyl, C1-C3 alkoxy, C1-C3 haloalkoxy, C1-C3 haloalkyl or C1-C3 alkyl optionally substituted with a C1-C3 alkoxy; or two R3, together with the carbon atom to which they are attached, join together to form an oxo group or a C3-C8 cycloalkyl; m is 0,1,2 or 3; R4 is phenyl, 5-6 membered heteroaryl, 3-10 membered heterocyclyl or C3-C8 cycloalkyl; wherein each R4 group is optionally substituted with 1-3 substituents independently selected from R6; R5 is hydrogen, halogen, cyano, hydroxyl, C1-C3 alkoxy, C1-C3 haloalkoxy, C1-C3 haloalkyl, -NRCRDo C1-C3 alkyl; and each R6 is independently selected from halogen; cyan; -CO2H; -NRERF; -(C=O)NRERF; C1-C3 alkoxy; C1-C3 haloalkyl; C1-C3 haloalkoxy; 5-6 membered heteroaryl optionally substituted with C1-C3 alkyl optionally substituted with hydroxyl, -NRERFo C1-C3 alkoxy; and 3-8 membered heterocyclyl; RA, RB, Rc, RD are independently hydrogen, C1-C3 alkyl, or RA, and RB, or Rcy RD, together with the nitrogen atom to which they are attached, join to form a 4-6 membered heterocyclyl; and REy RF are independently hydrogen, C1-C3 alkyl or REy RF, together with the nitrogen atom to which they are attached, join to form a 4-6 membered heterocyclyl optionally substituted with C1-C3 alkyl or C1-C3 alkoxy. QAFQCn / ZZnZ / q / ΥΙΛΙ In some embodiments, the five-membered nitrogen-containing ring, formed in part by X and Y, is a heteroaromatic ring. In some embodiments, X is C and Y is C. In some embodiments, X is N and Y is C. In some embodiments, X is C and Y is N. In some embodiments, Z is N. In some embodiments, Z is CR5. In some embodiments, X is C; Yes c; and Z is CR5. In some embodiments, X is N; Yes c; and Z is CR5. In some embodiments, X is C; Y is N; and Z is CR5. In some embodiments, X is C; Yes c; and Z is N. In some embodiments, X is N; Yes c; and Z is N. In some embodiments, X is C; Y is N; and ZesN. In some embodiments, R1 is hydrogen. In some embodiments, R1 is halogen, cyano, hydroxyl, C1-C3 alkoxy, C1-C3 haloalkyl, -NRARBo C1-C3 alkyl optionally substituted with 1-3 substituents independently selected from hydroxyl and C1-C3 alkoxy. In some embodiments, R1 is halogen or cyano. In some embodiments, R1 is chloro or cyano. In some embodiments, R1 is halogen. For example, R1 is fluoro. For example, R1 is chlorine. In some embodiments, R1 is cyan. In some embodiments, R1 is hydroxyl. In some embodiments, R1 is C1-C3 alkoxy. In some embodiments, R1 is methoxy or ethoxy. In some embodiments, R1 is C1-C3 haloalkoxy. In some embodiments, R1 is trifluoromethoxy, difluoromethoxy or fluoromethoxy. In some embodiments, R1 is C1-C3 haloalkyl. In some embodiments, R1 is trifluoromethyl or 2,2,2trifluoroethyl. In some embodiments, R1 is -NRARB. In some embodiments, RA and RB are independently hydrogen or C1-C3 alkyl. In certain embodiments, one of RAy RB is hydrogen and the other of RAy RB is C1-C3 alkyl. In some embodiments, one of RAy RB is hydrogen and the other of RAy RB is methyl. In some embodiments, one of RAy RB is hydrogen and the other of RAy RB is ethyl. In certain embodiments, both RA and RB are hydrogen. In certain embodiments, both RA and RB are C1-C3 alkyl. In some embodiments, both RA and RB are methyl. In some embodiments, one of RAy RB is methyl and the other of RAy RB is ethyl. In some embodiments, both RA and RB are ethyl. In some embodiments, RA and RB, along with the nitrogen atom to which they are attached, join together to form a 4-6 membered heterocyclyl. In certain embodiments, RA and RB, together with the nitrogen atom to which they are attached, join together to form a 4-membered heterocyclyl. In some embodiments, RA and RB, along with the nitrogen atom to which they are attached, join together to form a 5-membered heterocyclyl. In some embodiments, RA and RB, along with the nitrogen atom to which they are attached, join together to form a 6-membered heterocyclyl. In some embodiments, R1 is C1-C3 alkyl optionally substituted with 1-3 substituents independently selected from hydroxyl and C1-C3 alkoxy. In certain embodiments, R1 is C1-C3 alkyl optionally QRFQCn / ZZnZ / q / ΥΙΛΙ substituted with 1 substituent selected from hydroxyl and C1-C3 alkoxy. In some of these embodiments, R1 is methyl optionally substituted with 1 substituent selected from hydroxyl and C1-C3 alkoxy. In certain embodiments, R1 is ethyl optionally substituted with 1 substituent selected from hydroxyl and C1-C3 alkoxy. In certain embodiments, R1 is C1-C3 alkyl optionally substituted with hydroxyl. In certain embodiments, R1 is C1-C3 alkyl optionally substituted with C1-C3 alkoxy (e.g., methoxy). In some embodiments, R1 is hydroxymethyl or methoxyethyl. In some embodiments, R1 is C1-C3 unsubstituted alkyl (e.g., methyl or ethyl). In some embodiments, R2 is hydrogen. In some embodiments, R2 is halogen. For example, R2 is fluoro. For example, R2 is chlorine. In some embodiments, R2 is amino. In some embodiments, R2A is hydrogen. In some embodiments, R2A is halogen, for example, R2A is fluoro or chloro. In some embodiments, R2A is C1-C6 alkyl, such as those described herein. In some embodiments, n is 1, 2, or 3. In some embodiments, n is 1 or 2. In some embodiments, n is 2 or 3. In some embodiments, n is 1 or 3. In some embodiments, n is 1. In some embodiments, n is 2. In some embodiments, n is 3. In some embodiments, m is 0.1, 2 or 3. In some embodiments, m is 0.1 or 2. In some embodiments, m is 1.2 or 3. In some embodiments, m is 0.2 or 3. In some embodiments, m is 0, 1 or 3. In some embodiments, m is 0 or 1. In some embodiments, m is 0 or 2. In some embodiments embodiment, m is 0 or 3. In some embodiments, m is 1 or 2. In some embodiments, m is 1 or 3. In some embodiments, m is 2 or 3. In some embodiments, m is 0. In some embodiments, m is 1. In some embodiments, m is 2. In some embodiments, m is 3. In some embodiments, each R3 is independently halogen, cyano, C3-C6 cycloalkyl, C1-C3 alkyl optionally substituted with C1-C3 alkoxy or cyano, C1-C3 haloalkyl, C1-C3 alkoxy or C1-C3 haloalkoxy. In some embodiments, each R3 is independently C3-C6 cycloalkyl, C1-C3 alkyl optionally substituted with C1 C3 alkoxy or cyano, C1-C3 haloalkyl, C1-C3 alkoxy or C1-C3 haloalkoxy. In some embodiments, each R3 is independently C1-C3 haloalkyl or unsubstituted C1-C3 alkyl. In some embodiments, each R3 is independently cyclopropyl, methyl optionally substituted with methoxy, trifluoromethyl, methoxy or trifluoromethoxy. In some embodiments, each R3 is independently cyclopropyl, methyl, methoxymethyl or trifluoromethyl. In some embodiments, each R3 is independently hydroxyl, C3-C6 cycloalkyl, C1-C3 alkyl optionally substituted with C1-C3 alkoxy or C1-C3 haloalkyl. In some embodiments, each R3 is independently hydroxyl, cyclopropyl, methyl optionally substituted with methoxy or trifluoromethyl. In some embodiments, each R3 is independently hydroxyl, cyano, -NRARB, 5-6 membered heteroaryl optionally substituted with C1-C3 alkyl; C3-C6 cycloalkyl, C1-C3 alkyl optionally substituted with a C1-C3 alkoxy or a cyano, or C1-C3 haloalkyl. In some embodiments, each R3 is independently hydroxyl, C3C6 cycloalkyl, C1-C3 alkyl substituted with a C1-C3 alkoxy, or C1-C3 haloalkyl. In some embodiments, each R3 is independently hydroxyl, cyano, C3-C6 cycloalkyl, C1-C3 alkyl or C1-C3 haloalkyl. In some embodiments, each R3 is independently halogen. For example, an R3 is fluoro or chlorine. In some embodiments, each R3 is independently hydroxyl. In some embodiments, each R3 is independently C3-C6 cycloalkyl, C1-C3 alkyl, C1-C3 alkoxy, C1C3 haloalkoxy or C1-C3 haloalkyl. In some embodiments, each R3 is independently hydroxyl. In some embodiments, each R3 is independently cyano. In some embodiments, each R3 is independently C3-C6 cycloalkyl. In some embodiments, each R3 is independently C3-C5 cycloalkyl. In some embodiments, each R3 is independently cyclopropyl. In some embodiments, each R3 is independently C3-C6 cycloalkyl and m is 1 or 2. In some embodiments, when m is 2, one R3 is C3-C6 cycloalkyl and the other R3 is not C3-C6 cycloalkyl. In some embodiments, each R3 is independently -NRARB. In some embodiments, each R3 is independently -NRARB and m is 1 or 2. In some embodiments, when m is 2, one R3 is -NRARB and the other R3 is not -NRARB. In some embodiments, each R3 is independently 5-6 membered heteroaryl optionally substituted with C1-C3 alkyl. In some embodiments, each R3 is independently 5-6 membered heteroaryl optionally substituted with C1-C3 alkyl and m is 1 or 2. In some embodiments, when m is 2, one R3 is 5-6 membered heteroaryl optionally substituted with C1-C3 alkyl and the other R3no is 5-6 membered heteroaryl. In some embodiments, each R3 is independently 5-6 membered heteroaryl substituted with C1-C3 alkyl. In some embodiments, each R3 is independently 5-6 membered heteroaryl substituted with C1 C3 alkyl and m is 1 or 2. In some embodiments, when m is 2, one R3 is 5-6 membered heteroaryl substituted with C1-C3 alkyl and the other R3no is 5-6 membered heteroaryl. In some embodiments, each R3 is independently 5-6 membered heteroaryl. In some embodiments, each R3 is independently 5-6 membered heteroaryl and m is 1 or 2. In some embodiments, when m is 2, one R3 is 5-6 membered heteroaryl and the other R3 is not 5-6 membered heteroaryl. members. In some embodiments, each R3 is independently C1-C3 alkyl optionally substituted with a C1-C3 alkoxy or a cyano. In some embodiments, each R3 is independently C1-C3 alkyl. For example, an R3 is methyl or ethyl. In some embodiments, each R3 is independently C1-C3 alkyl substituted with a C1C3 alkoxy, such as methoxy, ethoxy, n-propoxy, or isopropoxy. In some embodiments, an R3 is methoxymethyl or methoxyethyl. In some embodiments, each R3 is independently C1-C3 alkyl substituted with a cyano group, such as cyanomethyl, or 1- or 2-cyanoethyl. In some embodiments, each R3 is independently C1-C3 alkoxy. For example, R3 is methoxy or ethoxy. In some embodiments, each R3 is independently C1-C3 haloalkoxy. For example, an R3 is trifluoromethoxy, difluoromethoxy or fluoromethoxy. In some embodiments, each R3 is independently C1-C3 haloalkyl. For example, each R3 is trifluoromethyl or 2,2,2-trifluoroethyl. In some embodiments, m is 1 and R3 is C1-C3 alkyl optionally substituted with C1-C3 alkoxy or cyano. In some embodiments, m is 2 and each R3 is independently C1-C3 alkyl optionally substituted with C1 QRQQcn / zznz / q / υιλι C3 alkoxy or cyano. In some embodiments, m is 1 and R3 is C1-C3 alkyl. In some embodiments, m is 2 and each R3 is independently C1-C3 alkyl. In some embodiments, m is 1 and R3 is C1-C3 alkyl substituted with C1-C3 alkoxy. In some embodiments, m is 2 and each R3 is independently C1-C3 alkyl substituted with C1-C3 alkoxy. In some embodiments, m is 1 and R3 is C1-C3 alkyl substituted with cyano. In some embodiments, m is 2 and each R3 is independently C1-C3 alkyl substituted with cyano. In some embodiments, m is 2 and each R3 is independently C1-C3 alkyl optionally substituted with C1-C3 alkoxy, the R3 groups are geminal C1-C3 alkyl groups, each optionally substituted with C1-C3 alkoxy. In some embodiments, each R3 is independently C1-C3 alkyl optionally substituted with C1-C3 alkoxy. In some embodiments, an R3 group is methyl or methoxymethyl. In some embodiments, each R3 is independently C1-C3 alkoxy. In some embodiments, each R3 is independently C1-C3 alkoxy and m is 1 or 2. In some embodiments, when m is 2, one R3 is C1-C3 alkoxy and the other R3 is not C1-C3 alkoxy. In some of these embodiments, the C1-C3 alkoxy is methoxy. In some embodiments, each R3 is independently C1-C3 haloalkoxy. In some embodiments, each R3 is independently C1-C3 haloalkoxy and m is 1 or 2. In some embodiments, when m is 2, one R3 is C1-C3 haloalkoxy and the other R3 is not C1-C3 haloalkoxy. In some of these embodiments, the C1-C3 haloalkoxy is trifluoromethoxy. In some embodiments, each R3 is independently C1-C3 haloalkyl. In some embodiments, each R3 is independently C1-C3 haloalkyl and m is 1 or 2. In some embodiments, when m is 2, one R3 is C1-C3 haloalkyl and the other R3 is not C1-C3 haloalkyl. In some of these embodiments, the C1-C3 haloalkyl is trifluoromethyl. In some embodiments, m is 2 and the R3 groups are geminal. In some embodiments, m is 2 and each R3 is independently C1-C3 haloalkyl. In some embodiments, the R3 groups are geminal independently selected C1-C3 haloalkyl groups. In some embodiments, m is 2, one R3 is C1-C3 alkyl optionally substituted with C1-C3 alkoxy or cyano, and the other R3 is C1-C3 haloalkyl. In some embodiments, m is 2, one R3 is C1-C3 alkyl substituted with C1-C3 alkoxy or cyano, and the other R3 is C1-C3 haloalkyl. In some embodiments, m is 2, one R3 is C1-C3 alkyl and the other R3 is C1-C3 haloalkyl. In some embodiments, the R3 groups are C1-C3 alkyl (optionally substituted with C1-C3 alkoxy or cyano) and C1-C3 haloalkyl groups. In some embodiments, the R3 groups are C1-C3 alkyl groups (substituted with C1-C3 alkoxy or cyano) and C1-C3 haloalkyl groups. In some embodiments, the R3 groups are geminal C1-C3 alkyl and C1-C3 haloalkyl groups. In some embodiments, m is 2, one R3 is C1-C3 alkyl, optionally substituted with C1-C3 alkoxy or cyano, and the other R3 is C3-C6 cycloalkyl. In some embodiments, m is 2, one R3 is C1-C3 alkyl substituted with C1-C3 alkoxy and the other R3 is C3-C6 cycloalkyl. In some embodiments, m is 2, one R3 is C1-C3 alkyl substituted with cyano and the other R3 is C3-C6 cycloalkyl. In some embodiments, m is 2, one R3 is C1-C3 alkyl and the other R3 is C3-C6 cycloalkyl. In some embodiments, the R3 groups are C1-C3 alkyl (optionally substituted with C1-C3 alkoxy or cyano) and C3-C6 cycloalkyl groups. In some embodiments, the R3 groups are C1-C3 alkyl (substituted with C1-C3 alkoxy or cyano) and C3-C6 cycloalkyl groups. In some embodiments, the R3 groups are geminal C1-C3 alkyl and C3-C6 cycloalkyl groups. In some embodiments, m is 2, one R3 is C1-C3 haloalkyl and the other R3 is C3-C6 cycloalkyl. In some embodiments, the R3 groups are C1-C3 haloalkyl and C3-C6 cycloalkyl groups. In some embodiments, m is 1 and R3 is methyl, methoxymethyl, trifluoromethyl or cyclopropyl. In some embodiments, m is 2 and each R3 is methyl. In some embodiments, m is 2 and each R3 is trifluoromethyl. In some embodiments, m is 2 and one R3 is methyl and the other R3 is methoxy. In some embodiments, m is 2 and one R3 is cyclopropyl and the other R3 is methoxy. In some embodiments, m is 1 and each R3 is methyl. In some embodiments, m is 2 and each R3 is methyl. In some embodiments, m is 2, each R3 is methyl and the R3 groups are geminal methyl groups. In some embodiments, each R3 is methyl. In some embodiments, m is 1 and R3 is methoxymethyl. In some embodiments, m is 2 and R3 is methyl. In some embodiments, m is 2 and R3 is methoxymethyl. In some embodiments, m is 2, each R3 is methyl and the R3 groups are geminal methyl groups. In some embodiments, m is 2 and the R3 groups are geminal methyl and methoxymethyl groups. In some embodiments, m is 2 and the R3 groups are geminal. In some embodiments, m is 2 and each R3 is trifluoromethyl. In some embodiments, the R3 groups are geminal trifluoromethyl groups. In some embodiments, m is 2, one R3 is C1-C3 alkyl, optionally substituted with C1-C3 alkoxy or cyano, and the other R3 is trifluoromethyl. In some embodiments, m is 2, one R3 is C1-C3 alkyl substituted with C1-C3 alkoxy, and the other R3 is trifluoromethyl. In some embodiments, m is 2, one R3 is C1-C3 alkyl and the other R3 is trifluoromethyl. In some embodiments, m is 2, one R3 is methyl and the other R3 is trifluoromethyl. In some embodiments, m is 2, one R3 is methoxymethyl and the other R3 is trifluoromethyl. In some embodiments, the R3 groups are geminal methyl and trifluoromethyl groups. In some embodiments, the R3 groups are geminal methoxymethyl and trifluoromethyl groups. In some embodiments, m is 2, one R3 is methyl and the other R3 is cyclopropyl. In some embodiments, m is 2, one R3 is methoxymethyl and the other R3 is cyclopropyl. In some embodiments, the R3 groups are geminal methyl and cyclopropyl groups. In some embodiments, the R3 groups are geminal methoxymethyl and cyclopropyl groups. In some embodiments, m is 2, one R3 is trifluoromethyl and the other R3 is cyclopropyl. In some embodiments, the R3 groups are geminal trifluoromethyl and cyclopropyl groups. In some embodiments, m is 2 and the two R3s, along with the carbon atom to which they are attached, join together to form an oxo group. In some embodiments, m is 2 and the two R3 join to form a C3-C8 cycloalkyl (for example, a cyclopropyl, cyclobutyl, cyclopentyl, cyclohexyl, cycloheptyl or cyclooctyl). In some embodiments, R4 is phenyl, naphthyl, 5-10 membered heteroaryl, 3-10 membered heterocyclyl or C3C8 cycloalkyl; wherein each R4 group is optionally replaced with 1-2 independently selected R6. In some embodiments, R4 is phenyl, 5-6 membered heteroaryl, 3-10 membered heterocyclyl or C3-C8 cycloalkyl; wherein each R4 group is optionally replaced with 1-2 independently selected R6. In some embodiments, R4 is phenyl, naphthyl, 5-10 membered heteroaryl, 3-10 membered heterocyclyl or C3-C8 cycloalkyl; wherein each R4 group is optionally replaced with 2-3 independently selected R6. In some embodiments, R4 is phenyl, naphthyl, 5-10 membered heteroaryl, 3-10 membered heterocyclyl or C3-C8 cycloalkyl; wherein each R4 group is optionally replaced with 1 or 3 independently selected R6. In some embodiments, R4 is phenyl, naphthyl, 5-10 membered heteroaryl, 3-10 membered heterocyclyl or C3-C8 cycloalkyl; wherein each R4 group is optionally replaced with 1 independently selected R6. In some embodiments, R4 is phenyl, naphthyl, 5-10 membered heteroaryl, 3-10 membered heterocyclyl or C3-C8 cycloalkyl; wherein each R4 group is optionally replaced with 2 independently selected R6. In some embodiments, R4 is phenyl, naphthyl, 5-10 membered heteroaryl, 3-10 membered heterocyclyl or C3-C8 cycloalkyl; wherein each R4 group is optionally replaced with 3 independently selected R6. In some embodiments, R4 is phenyl, 5-6 membered heteroaryl, 3-10 membered heterocyclyl or C3-C8 cycloalkyl; wherein each R4 group is optionally replaced with 2-3 independently selected R6. In some embodiments, R4 is phenyl, 5-6 membered heteroaryl, 3-10 membered heterocyclyl or C3-C8 cycloalkyl; wherein each R4 group is optionally replaced with 1 or 3 independently selected R6. In some embodiments, R4 is phenyl, 5-6 membered heteroaryl, 3-10 membered heterocyclyl or C3-C8 cycloalkyl; wherein each R4 group is optionally replaced with 1 independently selected R6. In some embodiments, R4 is phenyl, 5-6 membered heteroaryl, 3-10 membered heterocyclyl or C3-C8 cycloalkyl; wherein each R4 group is optionally replaced with 2 independently selected R6. In some embodiments, R4 is phenyl, 5-6 membered heteroaryl, 3-10 membered heterocyclyl or C3-C8 cycloalkyl; wherein each R4 group is optionally replaced with 3 independently selected R6. In some embodiments, R4 is phenyl or 5-membered heteroaryl; wherein each R4 group is optionally substituted with 1-3 substituents independently selected from R6. In some embodiments, R4 is phenyl or 6-membered heteroaryl; wherein each R4 group is optionally substituted with 1-3 substituents independently selected from R6. In some embodiments, R4 is naphthyl or 9-10 membered heteroaryl; wherein each R4 group is optionally substituted with 1-3 substituents independently selected from R6. In some embodiments, R4 is phenyl, 5-membered heteroaryl or cyclopentyl; wherein each R4 group is optionally substituted with 1-3 substituents independently selected from R6. In some embodiments, R4 is phenyl, 6-membered heteroaryl, cyclopentyl or cyclohexyl; wherein each R4 group is optionally substituted with 1-3 substituents independently selected from R6. In some embodiments, R4 is phenyl optionally substituted with 1-3 R6 independently selected. In certain embodiments, R4 is phenyl optionally substituted with 1 R6. In certain embodiments, R4 is phenyl optionally substituted with 2 independently selected R6. In certain embodiments, R4 is phenyl optionally substituted with 3 independently selected R6s. In some embodiments, R4 is unsubstituted phenyl. In some embodiments, R4 is phenyl substituted with 1-3 substituents selected independently from R6. In certain embodiments, R4 is phenyl substituted with R6. In certain embodiments, R4 is substituted phenyl QRQQcn / zznz / q / υιλι with 2 R6selected independently. In some embodiments, R4 is phenyl substituted with 3 independently selected R6s. In some embodiments, R4 is naphthyl optionally substituted with 1-3 independently selected R6. In some embodiments, R4 is naphthyl substituted with 1-3 independently selected R6. In some embodiments, R4 is unsubstituted naphthyl. In some embodiments, R4 is 5-6 membered heteroaryl optionally substituted with 1-3 (e.g., 2) substituents independently selected from R6. In some embodiments, R4 is 6-membered heteroaryl optionally substituted with 1-3 (e.g., 2) R6 independently selected. In some embodiments, R4 is 9-10 membered heteroaryl optionally substituted with 1-3 (e.g., 2) independently selected R6. In some embodiments, R4 is 9-membered heteroaryl optionally substituted with 13 (e.g., 2) R6 independently selected. In some embodiments, R4 is 10-membered heteroaryl optionally substituted with 1-3 (e.g., 2) independently selected R6. In some embodiments, R4 is unsubstituted 5-6 membered heteroaryl. In some embodiments, R4 is unsubstituted 9-10 membered heteroaryl. In some embodiments, R4 is substituted 5-6 membered heteroaryl with 1-3 substituents selected independently from R6. In some embodiments, R4 is 9-10 membered heteroaryl substituted with 1-3 substituents selected independently from R6. In some embodiments, the 5-6 membered heteroaryl is 3-pyridyl, 4-pyridyl, or 4-pyridazinyl. In some embodiments, the 5-6 membered R4heteroaryl is 3-pyridyl or 4-pyridyl. In some embodiments, the 5-6 membered R4heteroaryl is pyridonyl. In some embodiments, R4 is 3-10 membered heterocyclyl optionally substituted with 1-3 substituents independently selected from R6. In some embodiments, R4 is 6-10 membered heterocyclyl optionally substituted with 1-3 substituents independently selected from R6. In some embodiments, R4 is 3-10 membered heterocyclyl substituted with 1-3 substituents independently selected from R6. In some embodiments, R4 is 6-10 membered heterocyclyl substituted with 1-3 substituents selected independently from R6. In some embodiments, R4 is 3-10 membered heterocyclyl substituted with 1-2 substituents independently selected from R6. In some embodiments, R4 is 6-10 membered heterocyclyl substituted with 1-2 substituents selected independently from R6. In some embodiments, R4 is 3-10 membered heterocyclyl. In some embodiments, R4 is 6-10 membered heterocyclyl. In some embodiments, R4 is morpholino optionally substituted with 1-2 independently selected R6. In some embodiments, R4 is tetrahydropyranyl optionally substituted with 1-2 independently selected R6. In some embodiments, R4 is 1-oxaspiro[4.5]decane optionally substituted with 1-2 independently selected R6. In some embodiments, R4 is C3-C8 cycloalkyl optionally substituted with 1-3 independently selected R6. In certain embodiments, R4 is C3-C8 cycloalkyl optionally substituted with 1 R6. In certain embodiments, R4 is C3-C8 cycloalkyl optionally substituted with 2 independently selected R6. In certain embodiments, R4 is C3-C8 cycloalkyl optionally substituted with 3 independently selected R6. In some embodiments, R4 is unsubstituted C3-C8 cycloalkyl. In some embodiments, R4 is C3-C8 cycloalkyl substituted with 1-3 R6 independently selected. In certain embodiments, R4 is C3-C8 cycloalkyl substituted with 1 R6. In certain embodiments, R4 is C3-C8 cycloalkyl substituted with 2 independently selected R6. In certain embodiments, R4 is C3-C8 cycloalkyl substituted with 3 independently selected R6. In some embodiments, at least one of R6 is halogen. In some embodiments, at least one of R6 is fluoro. In some embodiments, at least one of R6 is chlorine. In some embodiments, one of R6 is halogen. In some embodiments, one of R6 is fluoro. In some embodiments, one of R6 is chlorine. In some embodiments, two of R6 are halogen. In some embodiments, two of R6 are fluoro. In some embodiments, two of R6 are chlorine. In some embodiments, three of R6 are halogen. In some embodiments, three of R6 are fluoro. In some embodiments, three of R6 are chlorine. In some embodiments, at least one of R6 is cyano. In some embodiments, at least one of R6 is hydroxyl. In some embodiments, at least one of R6 is -CO2H. In some embodiments, at least one of R6 is -N=(S=O)(C1-C3 alkyl)2. For example, at least one of R6 is -N=(S=O)(methyl)2. In some embodiments, at least one of R6 is -S(=O)P(C1-C3 alkyl) (e.g., -S(=O)p(methyl)). In some embodiments, at least one of R6 is -S(=O)(C1-C3 alkyl) (e.g., -S(=O)(methyl)). In some embodiments, at least one of R6 is -S(=O)2(C1-C3 alkyl) (e.g., -S(=O)2(methyl)). In some embodiments, p is 1. In some embodiments, p is 2. In some embodiments, at least one of R6 is -NRERF. In some embodiments, at least one of R6 is -(C=O)NRERF. In some embodiments, at least one of R6 is C1-C3 alkoxy optionally substituted with amino, hydroxyl or (C=O)NRERF. In some embodiments, at least one of R6 is C1-C3 unsubstituted alkoxy. In some embodiments, at least one of R6 is C1-C3 alkoxy substituted with amino, hydroxyl or -(C=O)NRERF. In some embodiments, at least one of R6 is C1-C3 alkoxy substituted with amino. In some embodiments, at least one of R6 is C1-C3 alkoxy substituted with hydroxyl. In some embodiments, at least one of R6 is C1-C3 alkoxy substituted with -(C=O)NRERF. In certain embodiments, at least one of R6 is methoxy or ethoxy. In some embodiments, RE and RF are independently hydrogen or C1-C3 alkyl. In certain embodiments, one of REy RF is hydrogen and the other of REy RF is C1-C3 alkyl. In some embodiments, one of REy RF is hydrogen and the other of REy RF is methyl. In some embodiments, one of REy RF is hydrogen and the other of REy RF is ethyl. In certain embodiments, both RE and RF are hydrogen. In certain embodiments, both RE and RF are C1-C3 alkyl. In some embodiments, both RE and RF are methyl. In some embodiments, one of REy RF is methyl and the other of REy RF is ethyl. In some embodiments, both RE and RF are ethyl. In some embodiments, RE and RF are independently hydrogen or C3-C6 cycloalkyl. In some embodiments, RE and RF are independently hydrogen or cyclopropyl. In some embodiments, one of REy RF is hydrogen and the other of REy RF is cyclopropyl. In some embodiments, RE and RF, together with the nitrogen atom to which they are attached, are linked to form a 4-6 membered heterocyclyl optionally substituted with C1-C3 alkyl or C1-C3 alkoxy. In certain embodiments, RE and RF, together with the nitrogen atom to which they are attached, join to form a 4-membered heterocyclyl optionally substituted with C1-C3 alkyl or C1-C3 alkoxy. In some embodiments, RE and RF, together with the nitrogen atom to which they are attached, join to form a 5-membered heterocyclyl optionally substituted with C1C3 alkyl or C1-C3 alkoxy. In some embodiments, RE and RF, together with the nitrogen atom to which they are attached, are linked to form a 6-membered heterocyclyl optionally substituted with C1-C3 alkyl or C1-C3 alkoxy. In some embodiments, RE and RF, together with the nitrogen atom to which they are attached, join to form a 4-6 membered heterocyclyl substituted with C1-C3 alkyl or C1-C3 alkoxy. In some embodiments, RE and RF, along with the nitrogen atom to which they are attached, join together to form a 4-6 membered heterocyclyl substituted with C1-C3 alkyl. In some embodiments, RE and RF, together with the nitrogen atom to which they are attached, join to form a 4-6 membered heterocyclyl substituted with C1-C3 alkoxy. In some embodiments, RE and RF, together with the nitrogen atom to which they are attached, join together to form an unsubstituted 4-6 membered heterocyclyl. In some embodiments, at least one of R6 is C1-C3 haloalkyl. In certain embodiments, at least one of R6 is trifluoromethyl, difluoromethyl or 2,2,2-trifluoroethyl. In certain embodiments, at least one of R6 is trifluoromethyl or 2,2,2-trifluoroethyl. In some embodiments, at least one of R6 is difluoromethyl. In some embodiments, at least one of R6 is C1-C3 haloalkoxy. In some embodiments, at least one of R6 is trifluoromethoxy. In some embodiments, at least one of R6 is difluoromethoxy. In some embodiments, at least one of R6 is 5-6 membered heteroaryl optionally substituted with 1-3 independently selected Rx. In some embodiments, at least one of R6 is 5-6 membered heteroaryl optionally substituted with 1-2 independently selected Rx. In some embodiments, at least one of R6 is 5-6 membered heteroaryl optionally substituted with 2-3 independently selected Rx. In some embodiments, at least one of R6 is 5-6 membered heteroaryl optionally substituted with 1 or 3 independently selected Rx. In some embodiments, at least one of R6 is 5-6 membered heteroaryl optionally substituted with 1 Rx. In some embodiments, at least one of R6 is 56-membered heteroaryl optionally substituted with 2 independently selected Rx. In some embodiments, at least one of R6 is 5-6 membered heteroaryl optionally substituted with 3 independently selected Rx. In some embodiments, at least one of R6 is 5-6 membered heteroaryl optionally substituted with halogen, cyano, hydroxyl, C1-C3 alkoxy, C1-C3 haloalkoxy, amino, C1-C3 haloalkyl or C1-C3 alkyl optionally substituted with hydroxyl or -NRERF. In some embodiments, R6 is 5-6 membered heteroaryl optionally substituted with C1-C3 alkyl optionally substituted with hydroxyl or -NRERF. In some embodiments, at least one of R6 is 5-6 membered heteroaryl optionally substituted with halogen, C1-C3 haloalkyl or C1-C3 alkyl optionally substituted with hydroxyl or -NRERF. In some embodiments, R6 is 5-6 membered heteroaryl substituted with C1-C3 hydroxyl substituted alkyl or -NRERF. In some embodiments, R6 is 56-membered heteroaryl substituted with hydroxymethyl, aminomethyl, hydroxyethyl, aminoethyl, propan-2-ol or propan-2-amine. In certain embodiments, at least one of R6 is 5-membered heteroaryl optionally substituted with 1-3 (e.g., 1-2, 2-3,1,2, or 3) independently selected Rx. In certain embodiments, at least one of R6 is a 5-membered heteroaryl optionally substituted with halogen, cyano, hydroxyl, C1-C3 alkoxy, C1-C3 haloalkoxy, C1C3 alkyl, amino or C1-C3 haloalkyl. In some embodiments, at least one of R6 is 6-membered heteroaryl optionally substituted with halogen, cyano, hydroxyl, C1-C3 alkoxy, C1-C3 haloalkoxy, amino, C1-C3 haloalkyl or C1C3 alkyl optionally substituted with hydroxyl or -NRERF . In some embodiments, R6 is 5-membered heteroaryl substituted with hydroxymethyl, aminomethyl, hydroxyethyl, aminoethyl, propan-2-ol or propan-2-amine. In some embodiments, R6 is 6-membered heteroaryl substituted with hydroxymethyl, aminomethyl, hydroxyethyl, aminoethyl, propan-2-ol or propan-2-amine. In some embodiments, at least one of R6 is unsubstituted 5-6 membered heteroaryl. In some embodiments, at least one of R6 is 1,2,3-triazol-2-yl. In some embodiments, each Rx is independently selected from cyano, hydroxyl, C1-C3 alkoxy or C1-C6 alkyl optionally substituted with 1-3 substituents independently selected from hydroxyl, C1-C3 alkoxy and NRGRH. In some embodiments, each Rx is independently selected from hydroxyl or C1-C6 alkyl optionally substituted with 1-3 substituents independently selected from hydroxyl, C1-C3 alkoxy and -NRGRH. In some embodiments, each Rx is independently selected from hydroxyl or C1-C2 alkyl optionally substituted with 1-3 (e.g., 1-2) substituents independently selected from hydroxyl, methoxy and dimethylamino. In some embodiments, each Rx is independently selected from hydroxyl or C1-C4 alkyl optionally substituted with 1-3 substituents independently selected from hydroxyl, C1-C3 alkoxy and -NRGRH. In some embodiments, RG and RH are independently hydrogen or C1-C3 alkyl. In certain embodiments, one is RGy RHes hydrogen and the other is RGy RHes C1-C3 alkyl. In some embodiments, one is made of RGy RHes hydrogen and the other is made of RGy RHes methyl. In some embodiments, one is made of RGy RHes hydrogen and the other is made of RGy RHes ethyl. In certain embodiments, both RG and RH are hydrogen. In certain embodiments, both RG and RH are C1-C3 alkyl. In some embodiments, both RG and RH are methyl. In some embodiments, one of RGy RHes methyl and the other of RGy RHes ethyl. In some embodiments, both RG and RH are ethyl. In some embodiments, RG and RH are independently hydrogen or C3-C6 cycloalkyl. In some embodiments, RG and RH are independently hydrogen or cyclopropyl. In some embodiments, one is made of RGy RHes hydrogen and the other is made of RGy RHes cyclopropyl. In some embodiments, RGy RH, together with the nitrogen atom to which they are attached, join to form a 4-6 membered heterocyclyl optionally substituted with C1-C3 alkyl or C1-C3 alkoxy. In certain embodiments, RGy RH, together with the nitrogen atom to which they are attached, join to form a 4-membered heterocyclyl optionally substituted with C1-C3 alkyl or C1-C3 alkoxy. In some embodiments, RGy RH, together with the nitrogen atom to which they are attached, join to form a 5-membered heterocyclyl optionally substituted with C1C3 alkyl or C1-C3 alkoxy. In some embodiments, RGy RH, together with the nitrogen atom to which they are attached, join to form a 6-membered heterocyclyl optionally substituted with C1-C3 alkyl or C1-C3 alkoxy. In some embodiments, RGy RH, together with the nitrogen atom to which they are attached, join to form a 4-6 membered heterocyclyl substituted with C1-C3 alkyl or C1-C3 alkoxy. In some embodiments, RGy RH, along with the nitrogen atom to which they are attached, join together to form a 4-6 membered heterocyclyl substituted with C1-C3 alkyl. In some embodiments, RGy RH, together with the nitrogen atom to which they are attached, join together to form a 4-6 membered heterocyclyl substituted with C1-C3 alkoxy. In some embodiments, RGy RH, together with the nitrogen atom to which they are attached, join together to form an unsubstituted 4-6 membered heterocyclyl. In some embodiments, at least one of R6 is C1-C3 alkyl optionally substituted with 1-2 substituents independently selected from hydroxyl, -NRERF, C1-C3 alkoxy and C3-C6 cycloalkyl. In some embodiments, at least one of R6 is C3-C6 cycloalkyl optionally substituted with hydroxyl. In some embodiments, at least one of R6 is C1-C3 alkyl optionally substituted with hydroxyl, -NRERFo C1-C3 alkoxy. In certain embodiments, at least one of R6 is methyl optionally substituted with hydroxyl, NRERFo C1-C3 alkoxy. In some embodiments, at least one of R6 is hydroxymethyl, 2-aminoethyl or methoxyethyl. In some embodiments, at least one of R6 is ethyl optionally substituted with hydroxyl, -NRERFo C1-C3 alkoxy. In some embodiments, RE and RF, together with the nitrogen atom to which they are attached, are linked to form a 4-6 membered heterocyclyl optionally substituted with C1-C3 alkyl or C1-C3 alkoxy. In certain embodiments, RE and RF, together with the nitrogen atom to which they are attached, join together to form a 4-membered heterocyclyl. In some embodiments, RE and RF, along with the nitrogen atom to which they are attached, join together to form a 5-membered heterocyclyl. In some embodiments, RE and RF, along with the nitrogen atom to which they are attached, join together to form a 6-membered heterocyclyl. In some embodiments, RE and RF, together with the nitrogen atom to which they are attached, join to form a 4-6 membered heterocyclyl substituted with C1-C3 alkyl or C1C3 alkoxy. In some embodiments, RE and RF, together with the nitrogen atom to which they are attached, join together to form an unsubstituted 4-6 membered heterocyclyl. In some embodiments, at least one of R6 is -(Q)q-3-8 membered heterocyclyl optionally substituted with independently selected 1-3 C1-C3 alkyl. In some embodiments, at least one of R6es-3-8 membered Oheterocyclyl optionally substituted with independently selected 1-3 C1-C3 alkyl. In some embodiments, at least one of R6 is -3-8 membered NH-heterocyclyl optionally substituted with independently selected 13 C1-C3 alkyl. In some embodiments, R6 is -(Q)q-3-8 membered heterocyclyl. In some embodiments, R6 is —(Q)q-3-8 membered heterocyclyl substituted with 1-3 C1-C3 alkyl. QRQQcn / zznz / q / υιλι independently selected. In some embodiments, R6 is -(Q)q-3-8 membered heterocyclyl substituted with C1-C3 alkyl. In some embodiments, R6 is -(Q)q-3-8 membered heterocyclyl substituted with independently selected 2 C1-C3 alkyl. In some embodiments, R6 is -(Q)q-3-8 membered heterocyclyl substituted with independently selected 3 C1-C3 alkyl. In some embodiments, q is 0. In some embodiments, q is 1. In some embodiments, Q is -O-. In some embodiments, Q is -NH-. In some embodiments, at least one of R6 is a 3-8 membered heterocyclyl. In certain embodiments, at least one of R6 is a 3-membered heterocyclyl. In certain embodiments, at least one of R6 is a 4-membered heterocyclyl. In certain embodiments, at least one of R6 is a 5-membered heterocyclyl. In certain embodiments, at least one of R6 is a 5-membered heterocyclyl comprising 1 heteroatom ring member selected from O, S and NH. In certain embodiments, at least one of R6 is tetrahydrofuranyl (e.g., 2-tetrahydrofuranyl). In certain embodiments, at least one of R6 is a 6-membered heterocyclyl. In certain embodiments, at least one of R6 is a 7-membered heterocyclyl. In certain embodiments, at least one of R6 is 8-membered heterocyclyl. In some embodiments, R4 is pyridyl, pyrimidinyl, pyrazinyl, pyrrolyl or imidazolyl; each of which is substituted with 2 R6: one R6 is triazolyl, imidazolyl, oxazolyl, pyrazolyl or pyrrolidinyl; and the other R6 is methoxy, trifluoromethyl, trifluoromethoxy, chloro or cyano. In some embodiments, R4 is pyridyl, pyrimidinyl or pyrazinyl; each of which is substituted with 2 R6: one R6 is triazolyl, imidazolyl, oxazolyl, pyrazolyl or pyrrolidinyl; and the other R6 is methoxy, trifluoromethyl, trifluoromethoxy, chloro or cyano. In some embodiments, R4 is pyridyl substituted with 2 R6: an R6 is triazolyl, imidazolyl or oxazolyl; and the other R6 is methoxy, trifluoromethyl, trifluoromethoxy, chloro or cyano. In some embodiments, R4 is pyridyl or phenyl; each of which is substituted with 2 R6: one R6 is triazolyl or pyrazolyl, each optionally substituted with hydroxymethyl, methyl, hydroxyl, hydroxyethyl, cyano or methoxy; and the other R6 is methoxy, trifluoromethyl, trifluoromethoxy, difluoromethyl, chloro or cyano. In some embodiments, R4 is 3-pyridyl or 4-pyridyl substituted with 1-3 R6 independently selected. ^R6 In some embodiments, R4 is the -C(=O)NH- portion of Formula (I). In some embodiments, R4 is -C(=O)NH- of Formula (I). , where the wavy line crosses the link connecting to the portion In some embodiments, R4 is, where the wavy line crosses the link connecting to the -C(=O)NH- portion of Formula (I). f In some embodiments, R4 is f 5 -C(=O)NH- of Formula (I). F X In some embodiments, R4 is -C(=O)NH- of Formula (I). R<t In some embodiments, R4 is the -C(=O)NH- portion of Formula (I). ’6, where the wavy line crosses the link that connects with the portion t6 A, where the wavy line crosses the link that connects with the portion O, where the wavy line crosses the link that connects with the R6 15 R 20 Xr A In some embodiments, when R4 is ú R® Xj R6 Xj or R6 is selected from the group consisting of cyano, halogen, C1-C3 haloalkyl and C1-C3 alkoxy QRFQCn / ZZnZ / q / ΥΙΛΙ X i i1 In some embodiments, when R4 is or 30 it consists of cyano, chloro, difluoromethyl, trifluoromethyl and methoxy. For example, when R4 is R6 vÓ 35 ú, R6 is C|oro or trifluoromethyl (e.g., chlorine). R6 is selected from the group that R6 AAn X^n In some embodiments, R4 is In some embodiments, R4 is the -C(=O)NH- portion of Formula (I). where the wavy line crosses the bond connecting with where the wavy line crosses the bond connecting with the -C(=O)NH- portion of Formula (I). In some embodiments, R4 is where the wavy line crosses the bond connecting to the -C(=O)NH- portion of Formula (I). In some embodiments, when R4 is Rθ^ R6A R6A is selected from the group consisting of: cyano, halogen, C1-C3 alkyl, C1-C3 alkoxy and C1-C3 haloalkyl; and R6B is selected from the group consisting of: 5-6 membered heteroaryl optionally substituted with cyano, amino or C1-C3 alkyl optionally substituted with hydroxyl or -NRERF; -(C=O)NRERF; C1-C3 alkoxy; C1-C3 haloalkyl; C1-C3 haloalkoxy; cyan; and C1-C3 alkyl. In some embodiments, when R4 is R6A is selected from the group consisting of: cyano, halogen, C1-C3 unsubstituted alkyl, C1-C3 alkoxy and C1-C3 haloalkyl; and R6B is selected from the group consisting of: 5-6 membered heteroaryl optionally substituted with cyano, hydroxyl, -N=(S=O)(C1-C3 alkyl)2, C1-C3 alkoxy, C1-C3 alkyl optionally substituted with 1 -2 substituents independently selected from hydroxyl, C1-C3 alkoxy and -NRGRH, or amino; -(C=O)NRERF; C1-C3 alkoxy; C1-C3 haloalkyl; C1-C3 haloalkoxy; cyan; C1-C3 alkyl; and —(Q)q-3-8 membered heterocyclyl optionally substituted with independently selected 1-3 C1-C3 alkyl. R6Ar6A R6B In some embodiments, when R4 is R6B QRQQcn / zznz / q / υιλι R6A is selected from the group consisting of: cyano, fluoro, chloro, methyl, ethyl, methoxy, trifluoromethyl; and R6B is selected from the group consisting of: 1,2,3-triazol-2-yl, 4-methyl-1,2,3-triazol-2-yl, 4-methyl-1,2,3-triazol-1 -yl, 4amino-1,2,3-triazol-2-yl, 5-cyano-1,2,3-triazol-1 -yl, 1,2,3-triazol-1-yl, 3-methyl-1 ,2,4-triazol-1-yl, 5-methyl-1,2,4-triazol-1-yl, 5-amino-1,2,4-triazol-1-yl, 1 -methyl-5-amino-1,2,4-triazol-3-yl, 1,2,4-triazol-4-on-2-yl, tetrazol-5-yl, 2-methyl-tetrazol-5-yl , 1-methyl-tetrazol-5-yl, imidazol-1-yl, 1-methyl-ímídazol-3-yl, 1-methyl-5-amino-ímídazol-3-yl, 3- methylmidazol-2-on-1-yl, 1-methylpyrazol-3-yl, 1-methylpyrazol-5-yl, pyrrol-1-yl, thiazol-2-yl, isothiazolid ¡n-2-¡l-1,1-dioxide, pyrrolidin-2-on-1-yl, oxazol-2-yl, oxadiazol-2-yl, 2-amino-pyrimidin-4- yl, -(C=O)4-methylperazin-1-yl, -(C=O)N(CH3)2, -(C=O)NHCH3, methoxy, ethoxy, difluoromethoxy, methyl, cyano. In some embodiments, when R4 is R6A is selected from the group consisting of: cyano, fluoro, chloro, methyl, ethyl, methoxy, trifluoromethyl; and R6B is selected from the group consisting of: 1,2,3-triazol-2-yl, 4-methyl-1,2,3-triazol-2-yl, 4-methyl-1,2,3-triazol-1 -yl, 4amino-1,2,3-triazol-2-yl, 5-cyano-1,2,3-triazol-1 -yl, 1,2,3-triazol-1-yl, 3-methyl-1 ,2,4-triazol-1-yl, 5-methyl-1,2,4-triazol-1-yl, 5-amino-1,2,4-triazol-1-yl , 1-methyl-5-amino-1,2,4-triazol-3-yl, 1,2,4-triazol-4-on-2-yl, tetrazol-5-yl, 2-methyl-tetrazol-5 -yl, 1methyl-tetrazol-5-yl, imidazol-1-yl, 1-methyl-ímídazol-3-yl, 1-methyl-5-amino-ímídazol-3-yl, 3-methyl¡midazol-2-on-1-yl, 1-methylpyrazol-3-yl, 1-methyl-pyrazol-5-yl, pyrrol-1-yl, thiazol-2-yl, isot ¡azol¡din-2-¡l-1,1-dioxide, pyrrolidin-2-on-1-yl, oxazol-2-yl, oxadiazol-2-yl, 2-amino-p¡ rimidin-4-yl, -(C=O)4-methylpiperazin-1-yl, -(C=O)N(CH3)2, -(C=O)NHCH3, methoxy, ethoxy, difluoromethoxy , trifluoromethyl, methyl and cyano. In some embodiments, when R4 is R6A is selected from the group consisting of: cyano, fluoro, chloro, methyl, ethyl, methoxy, difluoromethyl, trifluoromethyl; and R6B is selected from the group consisting of: 1,2,3-triazol-2-yl, 4-methyl-1,2,3-triazol-2-yl, 4-hydroxymethyl-1,2,3-tri azol-2-yl, 4-(1,2-dihydroxyethyl)-1,2,3-triazol-2-yl, 4-(1-hydroxyethyl)-1,2,3-triazole -2-Io, 4-methoxymethyl-1,2,3-triazol-2-yl, 4-methyl-1,2,3triazol-1-yl, 4-methoxy-1,2,3-triazol-2 -ílo, 4-amino-1,2,3-triazol-2-yl, 4-dimethylaminomethyl-1,2,3-triazol-2-yl, 5-cyano-1,2,3triazol-1-yl, 1,2,3-triazol-1-yl, 3-methyl-1,2,4-triazol-1-yl, 5-methyl-1,2,4-triazol-1-yl, 5-amino-1,2,4-triazol-1-yl, 1-methyl-5amino-1,2,4-triazol-3-yl, 1,2,4-triazol-4-on-2-yl, tetrazol-5-yl, 2-methyl-tetrazol-5-yl, 1-methyl-tetrazol-5-yl, imidazol-1-yl, pyrazol-1-yl, 5-cyano-pyrazol-1-yl , 1-methyl-imidazole-3-yl, 1-methyl-5-amino-imidazole-3-yl, 3-methylimidazole-2-on-1-yl, 1-methyl pyrazole-3 -yl, 1-methyl-pyrazol-5-yl, pyrrol-1-yl, thiazol-2-yl, isothiazol¡din-2-¡l-1,1 -dioxide, pyrrolidin- 2-on-1-yl, oxazol-2-yl, oxadiazol-2-yl, 2-amino-pyrimidin-4-yl, 2-tetrahydrofuranyl, -(C=O)4- methylperazin-1 -yl, -(C=O)N(CH3)2, -(C=O)NHCH3, N=(S=O)(methyl)2, methoxy, ethoxy, difluoromethoxy, methyl, cyano. > π N C K N C u σ In some embodiments, when R4 is R6A is selected from the group consisting of: cyano, chloro and trifluoromethyl; and R6B is selected from the group consisting of: 1,2,3-triazol-2-yl, 4-methyl-1,2,3-triazol-2-yl, 4-methyl-1,2,3-triazol-1yl, 4-amino-1,2,3-triazol-2-yl, 5-cyano-1,2,3-triazol-1-yl, 1,2,3-triazol-1-yl, 3- methyl-1,2,4-triazol-1-yl, 5-methyl1,2,4-triazol-1 -yl, 5-amino-1,2,4-triazol-1 -yl, 1-methyl-5- amino-1,2,4-triazol-3-yl and 1,2,4-triazol-4-on-2-yl. In some embodiments, when R4 is R6A is chlorine; and R6B is selected from the group consisting of: 1,2,3-triazol-2-yl, 1,2,3-triazol-1-yl and 1,2,4-triazol-4-on-2-yl. In some embodiments, R4 is , where the wavy line crosses the bond connecting to the -C(=O)NH- portion of Formula (I). R6A In some embodiments, R4esr6C, wherein the wavy line crosses the bond connecting to the -C(=O)NH- portion of Formula (I). In some embodiments, R4 is R6A , where the wavy line crosses the bond connecting to the -C(=O)NH- portion of Formula (I). In some embodiments, when R4 is R6A QRQQCn177(Υ7Γ1 / ΥΙΛΙ R6A is selected from the group consisting of: cyano, halogen, C1-C3 alkyl, C1-C3 alkoxy and C1-C3 haloalkyl; R6B is selected from the group consisting of: 5-6 membered heteroaryl optionally substituted with cyano, C1-C3 alkyl or amino; -(C=O)NRERF; C1-C3 alkoxy; C1-C3 haloalkyl; C1-C3 haloalkoxy; cyan; and C1-C3 alkyl; and R6C is selected from the group consisting of: cyano, halogen, C1-C3 alkyl, C1-C3 alkoxy, C1-C3 haloalkyl and -(Q)q-3-8 membered heterocyclyl optionally substituted with independently selected 1-3 C1-C3 alkyl. R6A / L,R6B In some embodiments, when R4 is * N R R6A is selected from the group consisting of: cyano, fluoro, chloro, methyl, ethyl, methoxy, trifluoromethyl; R6B is selected from the group consisting of: 1,2,3-triazol-2-yl, 4-methyl-1,2,3-triazol-2-yl, 4-methyl-1,2,3-triazol-1yl, 4-amino-1,2,3-triazol-2-yl, 5-cyano-1,2,3-triazol-1-yl, 1,2,3-triazol-1-yl, 3-methyl-1 ,2,4-triazol-1-yl, 5-methyl1,2,4-triazol-1 -yl, 5-amino-1,2,4-triazol-1-yl, 1-methyl-5-amino-1 ,2,4-triazol-3-yl, 1,2,4-triazol-4-on-2-yl, tetrazol5-yl, 2-methyl-tetrazol-5-yl, 1-methyl-tetrazol- 5-ílo, imidazol-1-yl, 1-methyl-imidazol-3-yl, 1-methyl-5-amino-imídazol-3yl, 3-methylimídazol-2-on-1-ílo, 1-methyl-pyrazol-3-yl, 1-methyl-pyrazol-5-yl, pyrrol-1-yl, thiazol-2-yl, isothiazolidin-2-yl1,1-dioxide, py rrolidin-2-on-1-yl, oxazol-2-yl, oxadiazol-2-yl, 2-amino-pyrimidin-4-yl, -(C=O)4-methylpiperazin-1yl, - (C=O)N(CH3)2, -(C=O)NHCH3, methoxy, ethoxy, difluoromethoxy, methyl, cyano; and R6C is selected from the group consisting of: cyano, fluoro, chloro, methyl, ethyl, methoxy, methyl, trifluoromethyl and pyrrolidin-3-yloxy. R6AA,R6B In some embodiments, when R4 is N R, R6A is selected from the group consisting of: cyano, chloro and trifluoromethyl; R6B is selected from the group consisting of: methoxy, 1,2,3-triazol-2-yl, 4-methyl-1,2,3-triazol-2-yl, 4-methyl-1,2,3triazol-1- yl, 4-amino-1,2,3-triazol-2-yl, 5-cyano-1,2,3-triazol-1-yl, 1,2,3-triazol-1 -yl, 3-methyl -1,2,4-triazol-1-yl, 5methyl-1,2,4-triazol-1-yl, 5-amino-1,2,4-triazol-1-yl, 1 -methyl-5-amino-1,2,4-triazol-3-yl and 1,2,4-triazol-4-on-2-yl; and R6C is selected from the group consisting of: cyano, chloro, methyl, trifluoromethyl and pyrrolidin-3-yloxy. R6A A^r6B In some embodiments, when R4 is N R, R6A is chlorine; R6B is selected from the group consisting of: methoxy, 1,2,3-triazol-2-yl, 1,2,4-triazol-4-on-2-yl; and R6C is selected from the group consisting of: cyano, chloro, methyl, trifluoromethyl and pyrrolidin-3-yloxy. QAFQCn / ZZnZ / q / ΥΙΛΙ In some embodiments, when R4 is R6A is selected from the group consisting of: cyano, halogen, C1-C3 alkyl, C1-C3 alkoxy and C1-C3 haloalkyl; R6B is selected from the group consisting of: 5-6 membered heteroaryl optionally substituted with cyano, C1-C3 alkyl or amino; -(C=O)NRERF; C1-C3 alkoxy; C1-C3 haloalkyl; C1-C3 haloalkoxy; cyan; and C1-C3 alkyl; and R6C is selected from the group consisting of: cyano, halogen, C1-C3 alkyl, C1-C3 alkoxy and C1-C3 haloalkyl. R6A R6A1^^r6B r^Á. ,r6bíl i ΤΎ In some embodiments, when R4 is or R R6A is selected from the group consisting of: cyano, fluoro, chloro, methyl, ethyl, methoxy, trifluoromethyl; R6B is selected from the group consisting of: 1,2,3-triazol-2-yl, 4-methyl-1,2,3-triazol-2-yl, 4-methyl-1,2,3-triazol-1yl, 4-amino-1,2,3-triazol-2-yl, 5-cyano-1,2,3-triazol-1-yl, 1,2,3-triazol-1-yl, 3-methyl-1 ,2,4-triazol-1-yl, 5-methyl1,2,4-triazol-1-yl, 5-amino-1,2,4-triazol-l-yl, 1-methyl-5-amino-1 ,2,4-triazol-3-yl, 1,2,4-triazol-4-on-2-yl, tetrazol5-yl, 2-methyl-tetrazol-5-yl, 1 -methyl-tetrazol-5- yl, imidazol-1-yl, 1 -methyl-imidazol-3-yl, 1-methyl-5-amino-ímidazol-3yl, 3-methylimidazol-2-on-1 -yl, 1 -methyl-pyrazol-3-yl, 1-methyl-pyrazol-5-yl, pyrrol-1-yl, thiazol-2-yl, isothiazolidin-2-yl1,1-dioxide, pyrrolidin- 2-on-1-yl, oxazol-2-yl, oxadiazol-2-yl, 2-amino-pyrimidin-4-yl, -(C=O)4-methylpiperazin-1yl, -(C=O )N(CH3)2, -(C=O)NHCH3, methoxy, ethoxy, difluoromethoxy, methyl, cyano; and R6C is selected from the group consisting of: cyano, fluoro, chloro, methyl, ethyl, methoxy, methyl and trifluoromethyl. r6a In some embodiments, when R4 is R6A is selected from the group consisting of: cyano, chloro and trifluoromethyl; R6B is selected from the group consisting of: 1,2,3-triazol-2-yl, 4-methyl-1,2,3-triazol-2-yl, 4-methyl-1,2,3-triazol-1yl, 4-amino-1,2,3-triazol-2-yl, 5-cyano-1,2,3-triazol-1-yl, 1,2,3-triazol-1-yl, 3-methyl-1 ,2,4-triazol-1-yl, 5-methyl 1,2,4-triazol-1 -lium, 5-amino-1,2,4-triazol-1 -lium, 1 -methyl-5-amino-1,2,4-triazol-3-yl and 1, 2,4-triazol-4-on-2-yl; and R6C is selected from the group consisting of: cyano, chloro, methyl and trifluoromethyl. QRFQCn / ZZnZ / q / ΥΙΛΙ r6A R6AT ~r6B R6¿ / R6Bf| ~Ί TV γγ AyN 6C In some embodiments, when R4 is or R R6A is chlorine; 10R6B is selected from the group consisting of: 1,2,3-triazol-2-yl and 1,2,4-triazol-4-on-2-yl; and R6C is selected from the group consisting of: cyano, chloro, methyl and trifluoromethyl. R6A Ty vVN'o6B In some embodiments, R4 is R, wherein the wavy line crosses the bond connecting to the -C(=O)NH- portion of Formula (I). R6AνΤχΚ 6B In some embodiments, when R4esR, R6A is selected from the group consisting of: cyano, halogen, C1-C3 alkyl, C1-C3 alkoxy and C1-C3 haloalkyl; R6B is selected from the group consisting of: C1-C3 alkyl and C1-C3 haloalkyl. r6a25JUCb In some embodiments, when R4esR, R6A is selected from the group consisting of: cyano, fluoro, chloro, methyl, ethyl, methoxy, trifluoromethyl; R6B is selected from the group consisting of: methyl, ethyl, difluoromethyl and trifluoromethyl; In some embodiments, when R4 is R6A R6A is chlorine; and R6B is selected from the group consisting of: trifluoromethyl and difluoromethyl. In some embodiments, R5 is hydrogen. In some embodiments, R5 is halogen. For example, R5 is fluoro. For example, R5 is chlorine. In some embodiments, R5 is cyan. In some embodiments, R5 is hydroxyl. In some embodiments, R5 is C1-C3 alkoxy. In some embodiments, R5 is methoxy or ethoxy. In some embodiments, R5 is C1-C3 haloalkoxy. In some embodiments, R5 is trifluoromethoxy, difluoromethoxy or fluoromethoxy. In some embodiments, R5 is C1-C3 haloalkyl. In some embodiments, R5 is trifluoromethyl or 2,2,2trifluoroethyl. In some embodiments, R5 is -NRCRD. In some embodiments, Rcy and RD are independently hydrogen or C1-C3 alkyl. In certain embodiments, one of Rcy RDes hydrogen and the other of Rcy RDes C1-C3 alkyl. In some embodiments, one of Rcy RDes hydrogen and the other of Rcy RDes methyl. In some embodiments, one of Rcy RDes hydrogen and the other of Rcy RDes ethyl. In certain embodiments, both Rc and RD are hydrogen. In certain embodiments, both Rc and RD are C1-C3 alkyl. In some embodiments, both Rc and RD are methyl. In some embodiments, one of Rcy RDes methyl and the other of Rcy RDes ethyl. In some embodiments, both Rc and RD are ethyl. In some embodiments, Rcy RD, along with the nitrogen atom to which they are attached, join together to form a 4-6 membered heterocyclyl. In certain embodiments, Rcy RD, along with the nitrogen atom to which they are attached, join together to form a 4-membered heterocyclyl. In some embodiments, Rcy RD, along with the nitrogen atom to which they are attached, join together to form a 5-membered heterocyclyl. In some embodiments, Rcy RD, along with the nitrogen atom to which they are attached, join together to form a 6-membered heterocyclyl. In some embodiments, R5 is C1-C3 alkyl. In some embodiments, R5 is methyl or ethyl. In some embodiments, X is N; Yes c; ZesN; R1 is halogen; R2 is hydrogen; R2A is hydrogen; m is 2 and R3 is independently C1-C3 alkyl or unsubstituted C1-C3 haloalkyl; n is 1;y R4 is 5-6 membered heteroaryl optionally substituted with 1-2 substituents independently selected from C1-C3 haloalkyl and 5-6 membered heteroaryl optionally substituted with 1-3 independently selected Rx. In some embodiments, R1 is chloro or fluoro. In some embodiments, R2 is hydrogen. In some embodiments, R2A is hydrogen. In some embodiments, each R3 is geminal. In some embodiments, one R3 is C1-C3 unsubstituted alkyl and the other R3 is C1-C3 haloalkoxy. In some embodiments, one R3 is methyl and the other R3 is trifluoromethyl. In some embodiments, R4 is unsubstituted 6-membered heteroaryl. In some embodiments, R4 is unsubstituted 1,2,3-triazolyl. In some embodiments, the compound of Formula (I) is a compound of Formula (II): where: n is 1 or 2; R1 is hydrogen, halogen, cyano, hydroxyl, C1-C3 alkoxy, C1-C3 haloalkoxy, C1-C3 haloalkyl, -NRARBo C1-C3 alkyl optionally substituted with 1-3 substituents independently selected from hydroxyl and C1-C3 alkoxy; R3A is halogen, hydroxyl, cyano, C3-C6 cycloalkyl, -NRARB, 5-6 membered heteroaryl optionally substituted with C1-C3 alkyl; C1-C3 alkoxy, C1-C3 haloalkoxy, C1-C3 haloalkyl or C1-C3 alkyl optionally substituted with a C1-C3 alkoxy or cyano; R3Bes halogen, hydroxyl, cyano, C3-C6 cycloalkyl, -NRARB, 5-6 membered heteroaryl optionally substituted with C1-C3 alkyl; C1-C3 alkoxy, C1-C3 haloalkoxy, C1-C3 haloalkyl or C1-C3 alkyl optionally substituted with a C1-C3 alkoxy or cyano; or R3A and R3B, together with the carbon atom to which they are attached, join together to form an oxo group or a C3-C8 cycloalkyl; each R6 is independently selected from halogen; cyan; hydroxyl; -CO2H; -N=(S=O)(C1-C3 alkyl)2, -S(=O)P(C1 C3 alkyl), -NRERF; -(C=O)NRERF; C1-C3 alkoxy optionally substituted with amino, hydroxyl or -(C=O)NRERF; C1-C3 haloalkyl; C1-C3 haloalkoxy; 5-6 membered heteroaryl optionally substituted with 1-3 independently selected Rx; C1-C3 alkyl optionally substituted with 1-2 substituents independently selected from hydroxyl, -NRERF, C1-C3 alkoxy and C3-C6 cycloalkyl; C3-C6 cycloalkyl optionally substituted with hydroxyl; and -(Q)qheterocyclyl 3-8 membered optionally substituted with independently selected 1-3 C1-C3 alkyl; p is 1 or 2; Qes -O-O-NH-; q is 0 or 1; each Rx is independently selected from halogen, cyano, hydroxyl, amino, C1-C3 alkoxy, C1-C3 haloalkoxy, C1-C3 haloalkyl or C1-C6 alkyl optionally substituted with 1-3 substituents independently selected from hydroxyl, C1-C3 alkoxy and - NRGRH; and RAy RB are independently hydrogen, C1-C3 alkyl, or RAy RB, together with the nitrogen atom to which they are attached, join to form a 4-6 membered heterocyclyl; and RE, RF, RGy RH are independently hydrogen, C1-C3 alkyl or C3-C6 cycloalkyl, or REy RF, or RGy RH, together with the nitrogen atom to which they are attached, join to form a 4-6 membered heterocyclyl optionally substituted with C1-C3 alkyl or C1-C3 alkoxy. In some embodiments of Formula (II): n is 1; R1 is hydrogen, halogen or cyano; one of R3A and R3Bes halogen, hydroxyl, cyano, C3-C6 cycloalkyl, C1-C3 alkoxy, C1-C3 haloalkoxy, C1-C3 haloalkyl or C1-C3 alkyl optionally substituted with a C1-C3 alkoxy or cyano; and the other of R3Ay R3Bes C1-C3 alkoxy, C1-C3 haloalkoxy, C1-C3 haloalkyl or C1-C3 alkyl optionally substituted with a C1-C3 alkoxy or cyano; each R6 is independently selected from halogen; cyan; hydroxyl; -CO2H; -N=(S=O)(C1-C3 alkyl)?, -S(=O)P(C1C3 alkyl), -NRERF; -(C=O)NRERF; C1-C3 alkoxy optionally substituted with amino, hydroxyl or -(C=O)NRERF; C1-C3 haloalkyl; C1-C3 haloalkoxy; 5-6 membered heteroaryl optionally substituted with 1-3 independently selected Rx; C1-C3 alkyl optionally substituted with 1-2 substituents independently selected from hydroxyl, -NRERF, C1-C3 alkoxy and C3-C6 cycloalkyl; and C3-C6 cycloalkyl optionally substituted with hydroxyl; p is 1 or 2; each Rx is independently selected from halogen, cyano, hydroxyl, amino, C1-C3 alkoxy, C1-C3 haloalkoxy, C1-C3 haloalkyl or C1-C6 alkyl optionally substituted with 1-3 substituents independently selected from hydroxyl, C1-C3 alkoxy and - NRGRH; and RE, RF, RGy RH are independently hydrogen, C1-C3 alkyl or C3-C6 cycloalkyl, or REy RF, or RGy RH, together with the nitrogen atom to which they are attached, join to form a 4-6 membered heterocyclyl optionally substituted with C1-C3 alkyl or C1-C3 alkoxy. In some embodiments of Formula (II): n is 2; R1 is hydrogen, halogen or cyano; one of R3A and R3Bes halogen, hydroxyl, cyano, C3-C6 cycloalkyl, C1-C3 alkoxy, C1-C3 haloalkoxy, C1-C3 haloalkyl or C1-C3 alkyl optionally substituted with a C1-C3 alkoxy or cyano; and the other of R3Ay R3Bes C1-C3 alkoxy, C1-C3 haloalkoxy, C1-C3 haloalkyl or C1-C3 alkyl optionally substituted with a C1-C3 alkoxy or cyano; each R6 is independently selected from halogen; cyan; hydroxyl; -CO2H; -N=(S=O)(C1-C3 alkyl)?, -S(=O)P(C1 C3 alkyl), -NRERF; -(C=O)NRERF; C1-C3 alkoxy optionally substituted with amino, hydroxyl or -(C=O)NRERF; C1-C3 haloalkyl; C1-C3 haloalkoxy; 5-6 membered heteroaryl optionally substituted with 1-3 independently selected Rx; C1-C3 alkyl optionally substituted with 1-2 substituents independently selected from hydroxyl, -NRERF, C1-C3 alkoxy and C3-C6 cycloalkyl; and C3-C6 cycloalkyl optionally substituted with hydroxyl; p is 1 or 2; each Rx is independently selected from halogen, cyano, hydroxyl, amino, C1-C3 alkoxy, C1-C3 haloalkoxy, C1-C3 haloalkyl or C1-C6 alkyl optionally substituted with 1-3 substituents independently selected from hydroxyl, C1-C3 alkoxy and - NRGRH; and RE, RF, RGy RH are independently hydrogen, C1-C3 alkyl or C3-C6 cycloalkyl, or REy RF, or RGy RH, together with the nitrogen atom to which they are attached, join to form a 4-6 membered heterocyclyl optionally replaced QRFQCn / ZZnZ / q / ΥΙΛΙ with C1-C3 alkyl or C1-C3 alkoxy. In some embodiments, the compound is a compound selected from Table 1, or a pharmaceutically acceptable salt thereof. Unless otherwise noted, (1) the stereochemical configuration of each stereocenter shown with dash-and-wedge bond notation and / or an adjacent CIP configuration is assumed to be relative; and (2) any stereocenter whose valency is filled with bonds that are not represented by dashes and wedges is a mixture of stereochemical configurations at that stereocenter. For example, compounds 3 and 4 are enantiomers, but it is not yet known which is the (R)-enantiomer and which is the (S)-enantiomer. In another example, compounds 33 and 34 are diastereomers in which the absolute configuration of the stereocenter attached to the trifluoromethyl is known, but the stereocenter in the tetrahydrofuryl group is relative (i.e., the tetrahydrofuryl stereocenter in one of compounds 33 and 34 has the (R) configuration, and the tetrahydrofuryl stereocenter in the other of compounds 33 and 34 has the (S) configuration). Table 1 Compound number Structure 1 Cl N ι Ν-Αζ N HN^O jO CI^Y N Ν' N 77 2 L F 7 fA / n=< hN? hn4° Cl- / / N'N. A 3 Cl \J ai? 0|·\^Ν νΛ nN 4 ci hnA0 CI\^=N nN 5 Cl V HN^O Xa cr y N N U 6 Cl = N=X in kN^N HN^O cr γ N N □«rocn / zznz / q / ΥΙΛΙ 7 o ^v o )=\ i 8 lí^vz z~z y o 9 Cl \ / N=( \ / 1 \ 11J HN^O οι-ψ ,N' N N XX □«rocn / zznz / q / ΥΙΛΙ □«rocn / zznz / q / ΥΙΛΙ QRQQcn / zznz / q / υιλι □«rocn / zznz / q / ΥΙΛΙ QAQQCn / 77n7 / q / ΥΙΛΙ absolute stereochemistry absolute stereochemistry absolute stereochemistry absolute stereochemistry absolute stereochemistry absolute stereochemistry absolute stereochemistry absolute stereochemistry 31 ' F f N' 1 1 N N ' N HN ' O ' ' . N N N N l. 32 1 1 Ν ’ 1 X N Λ 1 IN J O Cl N N N N 33 Cl 1 F N_. 1 X Ñ N N HN O <J N O The stereochemistry of the trifluoromethyl-bound stereocenter is absolute □«rocn / zznz / q / ΥΙΛΙ QRFQCn / ZZnZ / q / ΥΙΛΙ 37 Cl i' Absolute stereochemistry 38 IT ηνΆ / 0 Cl 1 / / N Absolute stereochemistry 39 ηνΛο c|-^yN Ν' h / / N Absolute stereochemistry 40 Cl ΗνΆ ¿y 0 FvJr7 F-7y=N Fn'K IV □«rocn / zznz / q / ΥΙΛΙ Absolute stereochemistry 41 Cl n^n ηνΆ h 0 Ν0^Ν N'N Absolute stereochemistry 42 r- Cl F\¿ - ​​N= / \A^n hnA0 ci^^n NC Absolute stereochemistry 43 Cl 1 1 N ' F \ N N N A 'J () Cl . N 1IO Absolute Stereochemistry 44 □«rocn / zznz / q / ΥΙΛΙ Cl > 1 N-- 1 N 0 ' Absolute stereochemistry 46 Cl 1 í N-· f V N N N HN ·' O c- . N O The stereochemistry of the stereocenter attached to the trifluoromethyl is absolute 47 QRFQCn / ZZnZ / q / ΥΙΛΙ / υιλι Cl 1 ’ N 1 \ N N ' N UN ' 0 α rN o The stereochemistry of the stereocenter attached to the trifluoromethyl is absolute 48 Cl 1 F N .-· 1 X N N -1 N UN O Cl . - N N J N HO Absolute stereochemistry 49 T \ O Absolute stereochemistry absolute stereochemistry QRQQcn / zznz / q / υιλι absolute stereochemistry absolute stereochemistry 53 ci FA - N= / N^N HNA r o The stereochemistry of the stereocenter attached to the trifluoromethyl is absolute 54 ci FA ~ N= / / y? ηνΆ F 0 E-JT / F^-^ The stereochemistry of the stereocenter attached to the trifluoromethyl is absolute 55 Cl fa - N= / N^N ην-Λ / 0 c|-^yN ho^oh The stereochemistry of the stereocenter attached to the trifluoromethyl is absolute □«rocn / zznz / q / ΥΙΛΙ QRFQCn / ZZnZ / q / ΥΙΛΙ Absolute stereochemistry 60 Cl ηνΆ / O fv4 / ¿ N Absolute stereochemistry 61 Cl V; ηνΛ0 F F Absolute stereochemistry 62 hnA0 c|-^yN n-n QRFQCn / ZZnZ / q / ΥΙΛΙ □«rocn / zznz / q / ΥΙΛΙ Absolute stereochemistry 67 o zX-.-1- Ή TI ° A C> Z / y / Z~2 Absolute stereochemistry 68 5 F F_V - zd Y N= / <V-N \ HN-^ \ / n o ho^W XF F F The stereochemistry of the stereocenter attached to trifluoromethyl is absolute 69 f. F F_V ' ,CI F ,N= / a yyr HN-y \ / =( 0 HO' N- / A~f F F The stereochemistry of the stereocenter attached to the trifluoromethyl is absolute 70 Cl F\T - n=< nx in” HN4 / 0 cl^yN Ν' ΗΟ^Ί ÓH □«rocn / zznz / q / ΥΙΛΙ QAQQCn / 77n7 / q / ΥΙΛΙ QAQQCn / 77n7 / q / ΥΙΛΙ □«rocn / zznz / q / ΥΙΛΙ □«rocn / zznz / q / ΥΙΛΙ Cl u 87 HN NcT^ N. / N 'VN UN U Absolute stereochemistry \ T 88 HN' ¿ N nX Ό R F y h 89 HN' Fv / / ¿ N-7 xo fU , N= F AX F 7 90 TU \\ \z Absolute stereochemistry □«rocn / zznz / q / ΥΙΛΙ 100 absolute stereochemistry absolute stereochemistry absolute stereochemistry 101 absolute stereochemistry absolute stereochemistry absolute stereochemistry 102 100 absolute stereochemistry 103 / υιλι 105 108 Cl FJ. N= / N^N hnAo / \==N F / Λ0 / o Absolute stereochemistry 109 ci vCn hn-4 “í o h2n °^y-N o / F The stereochemistry of both stereocenters is absolute 110 ci - N=K \ ΗνΆ N —i / O Ά-ίΑ 0 \-N í / V-F o / F Absolute stereochemistry 111 Cl FvF- n=K in HN^ ~~N 7 ° Ό—C N rF F The stereochemistry of both stereocenters is absolute QAFQCn / ZZnZ / q / ΥΙΛΙ 106 112 Cl Λ ΗΝ-Λ Fy Ν'ν Absolute stereochemistry 113 Cl ΗΝ-Λ L 0 / y^N F / Co>O Absolute stereochemistry 114 ΗΝ-Λ / 0 115 hnA0 FvA> / n-n □«rocn / zznz / q / ΥΙΛΙ 107 116 Cl \Γ - N=( N^N ηνΆ j 0 F / —sx xo The stereochemistry of the stereocenter attached to the trifluoromethyl is absolute 117 Cl F\T - n=< ΗνΆ ” / 0 F / 0 The stereochemistry of the stereocenter attached to the trifluoromethyl is absolute 118 Cl - N=( :N ΗνΆ / o clyN Absolute stereochemistry □«rocn / zznz / q / ΥΙΛΙ 108 119 120 ζ-ζ ΖΑ χ) ΆΑ° ί, ζ 121 c Cl A? χ 1ΝΛ Ά X ο-% Μ Yf F F Absolute stereochemistry 122 C| ηνΧ X 0 \JX / Vn F / 0==% N / Absolute stereochemistry □«rocn / zznz / q / ΥΙΛΙ 109 123 Cl HN-A L or FS ciVn / 0 Absolute stereochemistry 124 HN4 “ / 0 y=N 125 '; 1 HN-y l 0 '^\=^N □«rocn / zznz / q / ΥΙΛΙ 111 129 Cl :λ ηνΆ or Ν' IUN 130 Cl Ce? \ ηνΆ N—i / O N^yF F Absolute stereochemistry 131 Cl hn-4 J / 0 \ NH f>Yn Absolute stereochemistry 132 Cl y. ΗΝ-Λ Jj 0 \ Η )^Ν νΆ iUN Absolute stereochemistry QRFQCn / ZZnZ / q / ΥΙΛΙ 112 133 c Cl H / N HNA °Λ The stereochemistry of both stereocenters is absolute 134 \\ Q-ύ o 135 ':7 ηνΛ0 c|-^yN νΆ LUN 136 Cl y·' hn-A0 c|-^yN ν- Λ 113 Cl jy-'F 137 \ J HN—X / 0 R F n-n Cl N={F^f j^Kf 138 ΗΝΛ / 0 R F n-n SF r N F Xf >N 139 ηνΆ J 0 ci- / Λ N |l ,Ν rF >N 140 hn-4 / O Cl- / / N || -N □«rocn / zznz / q / ΥΙΛΙ 114 141 ηνΆ / 0 F / N'N 142 W' hnA0 V-O / n-n 143 ci % HN-A X / 0 n^f F Absolute stereochemistry 144 F F ,CI HN^ / 0 / n-n QRQQcn / zznz / q / υιλι 115 145 F F / Cl HN^ J / 0 / n-n 146 o αΛ H absolute □«rocn / zznz / q / ΥΙΛΙ 116 117 152 ϊ ϊ ηνΑ0 ν-ν 153 ο 71 Ο \ / X Ή \\ Λ=ζ 154 01 ΗΝ'Λ ν’ / ο n^f F Absolute stereochemistry 155 ηνΆ / 0 Yvn □«rocn / zznz / q / ΥΙΛΙ 118 156 w ηνΆ / 0 Vvn 157 o Z zX.3· H TI \ / X V—π b^Z\ Y ,z~z z—¿Jl z I M 158 o ha H V —11 cyz\ / ' y z^íjl z T ΙΌ 159 vu ΗΝ-Ά / 0 Cl-^ L> QRFQCn / ZZnZ / q / ΥΙΛΙ 160 Cl^N N'Nv 161 ηνΆ \A 0 nCA N rF F Absolute stereochemistry 162 HN4 “ / o vA / \=N F / N^\ Absolute stereochemistry 163 C| ηνΆ Absolute stereochemistry □«rocn / zznz / q / ΥΙΛΙ 120 164 οι F\ / _ N= / γ hnY J / 0 Absolute stereochemistry 165 r- Cl F\¿ - ​​N=K ηνΆ ? O F The stereochemistry of the stereocenter attached to the trifluoromethyl is absolute 166 Cl hnY Jj o F-Ύ F The stereochemistry of the stereocenter attached to the trifluoromethyl is absolute 121 167 Cl Fj. N=< ηνΆ / 0 α\=Ν -Νχ__ / ° The stereochemistry of the stereocenter attached to the trifluoromethyl is absolute 168 Cl N^N ηνΆ / 0 cl'^y=N l—r 0H Absolute stereochemistry 169 Cl Fs, , N= / F^V \ ηνΆ N—0 N-Á / / H N^V-F F^ F Absolute stereochemistry QAQQCn / 77n7 / q / ΥΙΛΙ 122 170 Cl - N=K n-Vn ΗνΆ / 0 The stereochemistry of the stereocenter attached to the trifluoromethyl is absolute 171 ci F^? hn-A / 0 Λ~\..>οη Absolute stereochemistry 172 ci F\ / _ N= / Wn ηνΆ P Absolute stereochemistry 173 ci F\¿ - ​​ηνΆ / 0 The stereochemistry of the stereocenter attached to the QAQQCn / 77n7 / q / ΥΙΛΙ 123 trifluoromethyl is absolute 174 Cl F\ / _ n^n ηνΆ J 0 The stereochemistry of the stereocenter attached to trifluoromethyl is absolute 175 Cl F\ / - NH2\A^N Γ νΆ Y 0 F F Absolute stereochemistry QRFQCn / ZZnZ / q / ΥΙΛΙ 124 176 Cl FU. N=( ηνΊ / 0 N=\ N= / x Absolute stereochemistry 177 Cl - NA F AV Ύ nh2 <nA^n ν' νΊ >N ° F \ F Absolute stereochemistry 178 C F\¿ - ​​n={N^N \ ηνΊ N—] / 0 L_J nA F Absolute stereochemistry 179 Cl A N=a n^n ΗΝ-Ί J / 0 \ s F Absolute stereochemistry □«rocn / zznz / q / ΥΙΛΙ □«rocn / zznz / q / ΥΙΛΙ □«rocn / zznz / q / ΥΙΛΙ / υιλι 128 189 190 191 The stereochemistry of the stereocenter attached to the trifluoromethyl is absolute 129 192 Cl ηνΆ / O n-A \ JJ / H NN LUN Absolute stereochemistry 193 Orí ηνΆ / 0 C|-^y=N n-n. 194 ΗΝ-Ά / 0 r Vn 195 hnAo Fv-O / Nn QAFQCn / ZZnZ / q / ΥΙΛΙ 130 □«rocn / zznz / q / ΥΙΛΙ 131 132 QRQQcn / zznz / q / υιλι 133 208 HN-Á ___ / θ \=N hoYnT 209 Cl - n=K hnA0 Absolute stereochemistry 210 F. F / Cl YW y νΎν ηνΆ / 0 TV 211 F F / Cl y W <j(N ' νΎν YVN Preparation processes Provided herein is a process for preparing a compound of Formula (I) (e.g., any compound described herein), comprising: react a compound of the formula (l-A) 134 with R4-NH2; to form a compound of Formula (I). In some embodiments, reacting the compound of Formula (l-A) with R4-NH2 comprises reacting one of the compounds of Formula (l-A) and R4-NH2 with a carbonyl equivalent to form an intermediate and then reacting the other of the compounds of the Formula (l-A) and R4-NH2 with the intermediate. In some of these embodiments, reacting the compound of Formula (l-A) with R4-NH2 comprises reacting R4-NH2 with a carbonyl equivalent to form the intermediate and then reacting the compound of Formula (l-A) with the intermediary. In any of the above embodiments, carbonyl equivalent refers to a reagent that replaces an N-H group in the compound of Formula (1-A) and / or R4-NH2 with a carbonyl moiety. Non-limiting examples of carbonyl equivalents include triphosgene and bis(trichloromethyl)carbonate. In some embodiments, reacting the compound of Formula (l-A) with R4-NH2 comprises reacting one of the compounds of Formula (l-A) and R4-NH2 with a carbonyl equivalent selected from triphosgene and bis(trichloromethyl) carbonate to form an intermediate and then react the other of the compounds of Formula (l-A) and R4-NH2 with the intermediate. In some of these embodiments, reacting the compound of Formula (l-A) with R4-NH2 comprises reacting R4-NH2 with a carbonyl equivalent selected from triphosgene and bis(trichloromethyl)carbonate to form the intermediate and then reacting the compound of the Formula (l-A) with the intermediate. In some embodiments, the carbonyl equivalent is triphosgene. In some embodiments, the carbonyl equivalent is bis(trichloromethyl)carbonate. Provided herein is a process for preparing a compound of Formula (I) (e.g., any compound described herein), comprising: react a compound of the formula (l-A) with R4-C(O)OH; to form a compound of Formula (I). In some embodiments, reacting the compound of Formula (l-A) with R4-C(O)OH comprises reacting R4-C(O)OH with diphenylphosphoryl azide (e.g., to form an intermediate (e.g., R4 -C(O))N3)) and 135 then heat (to, for example, form a second intermediate (for example, R4-N=C=O)) in the presence of the compound of Formula (l-A) to form the compound of Formula (I). In some embodiments, the compound of Formula (l-A) is a compound of Formula (l-A-N): R2 In some embodiments, when the compound of Formula (l-A) is a compound of Formula (l-A-N), the process further comprises reacting a compound of Formula (l-A-N-i) with a compound of the formula (l-A-N-ii) R2 to form the compound of the Formula (l-A-N). In certain embodiments, the reaction of the compound of Formula (l-A-N-i) with the compound of Formula (l-AN-ii) is carried out in the presence of an acid, such as an organic or inorganic acid. In some embodiments, the acid is hydrochloric acid or acetic acid. In some embodiments, the compound of Formula (l-A) is a compound of Formula (l-A-M): R2 In some embodiments, when the compound of Formula (l-A) is a compound of Formula (l-A-M), the process further comprises reacting a compound of Formula (l-A-M-i) 136 to form the compound of Formula (l-A-M). In some of these embodiments, the compound of Formula (l-A-M-i) is reacted with an iron salt, a silane, a peroxide and an acid to form the compound of Formula (l-A-M). In some embodiments, the iron salt is ferric (Z)-4-oxopent-2-en-2-olate. In some embodiments, the silane is phenylsilane. In some embodiments, the peroxide is 2-tert-butylperoxy-2-methyl-propane. In some embodiments, the acid is 2,2,2-trifluoroacetic acid. Treatment methods Some embodiments provide a method of treating an autoimmune disorder (e.g., a MALT1-associated autoimmune disorder) in a subject in need of such treatment, wherein the method comprises administering to the subject an effective amount of a compound of Formula (I ), or a pharmaceutically acceptable salt thereof, or a pharmaceutical composition thereof. In some embodiments, the autoimmune disorder is rheumatoid arthritis, multiple sclerosis, or systemic lupus erythematosus (SLE). Some embodiments provide a method of treating an inflammatory disorder (e.g., a MALT1-associated inflammatory disorder) in a subject in need of such treatment, wherein the method comprises administering to the subject an effective amount of a compound of Formula (I ), or a pharmaceutically acceptable salt thereof, or a pharmaceutical composition thereof. In some embodiments, the inflammatory disorder is a chronic graft versus host disease (cGVHD). Some embodiments provide a method of treating a type of cancer (e.g., a MALT1-associated cancer) in a subject in need of such treatment, wherein the method comprises administering to the subject an effective amount of a compound of the Formula (I), or a pharmaceutically acceptable salt thereof, or a pharmaceutical composition thereof. For example, provided herein are methods for treating a type of MALT1-associated cancer in a subject in need of such treatment, wherein the method comprises a) detecting a deregulation of a MALT 1 gene, a MALT 1 protease, or the expression , activity or level of any of these in a sample from the subject; and b) administering an effective amount of a compound of Formula (I), or a pharmaceutically acceptable salt thereof. In some embodiments, deregulation of a MALT1 gene, a MALT1 protease, or the expression, activity or level of any of these includes one or more fusion proteins. In some embodiments of any of the methods or uses described herein, the type of cancer (e.g., MALT1-associated cancer) is a type of hematological cancer. In some embodiments of any of the methods or uses described herein, the type of cancer (e.g., MALT1-associated cancer) is a solid tumor. In some embodiments of any of the methods or uses described herein, the type of cancer (e.g., MALT1-associated cancer) is a type of lung cancer (e.g., small cell lung carcinoma or lung cancer). non-small cell lung), thyroid cancer (for example, papillary thyroid cancer, medullary thyroid cancer (for example, sporadic medullary thyroid cancer or hereditary medullary thyroid cancer), differentiated thyroid cancer, recurrent thyroid cancer or refractory differentiated thyroid cancer), thyroid adenoma 137 thyroid, endocrine gland neoplasms, lung adenocarcinoma, bronchial lung cell carcinoma, multiple endocrine neoplasia type 2A or 2B (MEN2A or MEN2B, respectively), pheochromocytoma, parathyroid hyperplasia, breast cancer, breast carcinoma, breast neoplasia, colorectal cancer (for example, metastatic colorectal cancer), papillary renal cell carcinoma, ganglioneuromatosis of the gastroenteric mucosa, inflammatory myofibroblastic tumor, or cervical cancer. In some embodiments of any of the methods or uses described herein, the type of cancer (e.g., MALT1-associated cancer) is selected from the group of: acute lymphoblastic leukemia (ALL), acute myeloid leukemia (AML), adolescent cancer, adrenocortical carcinoma, anal cancer, appendix cancer, astrocytoma, atypical teratoid / rhabdoid tumor, basal cell carcinoma, bile duct cancer, bladder cancer, bone cancer, brain stem glioma, brain tumor, breast cancer, bronchial tumor, Burkitt lymphoma, carcinoid tumor, carcinoma of unknown primary site, cardiac tumors, cervical cancer, childhood cancers, chordoma, chronic lymphocytic leukemia (CLL), chronic myelogenous leukemia (CML), neoplasms chronic myeloproliferative, neoplasms by site, neoplasms, colon cancer, colorectal cancer, craniopharyngioma, cutaneous T-cell lymphoma, cutaneous angiosarcoma, bile duct cancer, ductal carcinoma in situ, embryonal tumors, endometrial cancer, ependymoma, esophageal cancer , esthesioneuroblastoma, Ewing sarcoma, extracranial germ cell tumor, extragonadal germ cell tumor, extrahepatic bile duct cancer, eye cancer, fallopian tube cancer, fibrous histiocytoma of bone, gallbladder cancer, gastric cancer, tumor gastrointestinal carcinoid, gastrointestinal stromal tumors (GIST), germ cell tumor, gestational trophoblastic disease, glioma, hairy cell tumor, hairy cell leukemia, head and neck cancer, thoracic neoplasms, head and neck neoplasms, CNS tumor , primary CNS tumor, heart cancer, hepatocellular cancer, histiocytosis, Hodgkin lymphoma, hypopharyngeal cancer, intraocular melanoma, islet cell tumors, pancreatic neuroendocrine tumors, Kaposi sarcoma, kidney cancer, Langerhans cell histiocytosis , laryngeal cancer, leukemia, lip and oral cavity cancer, liver cancer, lung cancer, lymphoma, macroglobulinemia, malignant fibrous histiocytoma of bone, osteocarcinoma, melanoma, Merkel cell carcinoma, mesothelioma, metastatic squamous neck cancer, middle tract carcinoma, oral cancer, multiple endocrine neoplasia syndromes, multiple myeloma, mycosis fungoides, myelodysplastic syndromes, myelodysplastic / myeloproliferative neoplasms, neoplasms by site, neoplasms, myelogenous leukemia, myeloid leukemia, multiple myeloma, myeloproliferative neoplasms, cavity cancer nasal and paranasal sinus, nasopharyngeal cancer, neuroblastoma, non-Hodgkin lymphoma, non-small cell lung cancer, lung neoplasm, lung cancer, lung neoplasms, respiratory tract neoplasms, bronchogenic carcinoma, bronchial neoplasms, oral cancer, breast cancer oral cavity, lip cancer, oropharyngeal cancer, osteosarcoma, ovarian cancer, pancreatic cancer, papillomatosis, paraganglioma, paranasal sinus and nasal cavity cancer, parathyroid cancer, penile cancer, pharyngeal cancer, pheochromositoma, pituitary cancer , plasma cell neoplasia, pleuropulmonary blastema, pregnancy-associated breast cancer, primary lymphoma of the central nervous system, primary peritoneal cancer, prostate cancer, rectal cancer, colon cancer, colon neoplasms, renal cell cancer, rhabdomyosarcoma, salivary gland cancer, sarcoma, Sézary syndrome, skin cancer, Spitz tumors, small cell lung cancer, cancer 138 small intestine, soft tissue sarcoma, squamous cell carcinoma, squamous neck cancer, stomach cancer, T-cell lymphoma, testicular cancer, throat cancer, thymoma and thymic carcinoma, thyroid cancer, renal pelvis transition, carcinoma of unknown primary site, urethral cancer, uterine cancer, uterine sarcoma, vaginal cancer, vulvar cancer, and Wilms tumor. In some embodiments, the type of cancer is a type of hematological cancer, such as a leukemia or lymphoma. In some embodiments, a type of hematological cancer (for example, hematological cancer types that are MALT1-associated cancer types) is selected from the group consisting of leukemias, lymphomas (non-Hodgkin lymphoma), Hodgkin disease (also called Hodgkin lymphoma) and myeloma, for example, acute lymphocytic leukemia (ALL), acute myeloid leukemia (AML), acute promyelocytic leukemia (APL), chronic lymphocytic leukemia (CLL), chronic myeloid leukemia (CML), chronic myelomonocytic leukemia (CMML ), chronic neutrophilic leukemia (CNL), acute undifferentiated leukemia (AUL), anaplastic large cell lymphoma (ALCL), prolymphocytic leukemia (PML), juvenile myelomonocytic leukemia (JMML), adult T-cell ALL, AML with trilineage myelodysplasia ( AML / TMDS), mixed lineage leukemia (MLL), myelodysplastic syndromes (MDS), myeloproliferative disorders (MPD), and multiple myeloma (MM). Additional examples of hematological cancer types include myeloproliferative disorders (MPD), such as polycythemia vera (PV), essential thrombocytopenia (ET), and idiopathic primary myelofibrosis (IMF / IPF / PMF). In some embodiments, the hematological cancer type (e.g., the hematological cancer type that is a MALT1-associated cancer type) is AML or CMML. In some embodiments, the type of cancer is glioblastoma, chronic myelogenous leukemia, myeloid leukemia, or non-Hodgkin lymphoma. In some embodiments, the type of cancer (e.g., MALT1-associated cancer type) is a solid tumor. Examples of solid tumors (e.g., solid tumors that are MALT 1-associated cancers) include, for example, lung cancer (e.g., lung adenocarcinoma, small cell lung carcinoma), pancreatic cancer, pancreatic ductal cancer, breast cancer, colon cancer, colorectal cancer, prostate cancer, renal cell carcinoma, neuroblastoma and melanoma. See, for example, Jiang etal., Cancer Research 2011, 71, 2183-2192; see also, Pan etal., Mol Cancer Res 2016,14, 93-102 and Penas et al., Blood 2010,115,2214-2219. In some embodiments, the subject is a human being. The compounds of Formula (I) and pharmaceutically acceptable salts thereof are also useful for treating a type of MALT1-associated cancer. The compounds of Formula (I) and pharmaceutically acceptable salts thereof are also useful for treating an autoimmune disorder associated with MALT 1. The compounds of Formula (I) and pharmaceutically acceptable salts of these are also useful for treating a MALT1-associated inflammatory disease. Accordingly, also provided herein is a method of treating a subject diagnosed with, or identified as having, a type of MALT 1-associated cancer, for example, any of the exemplary MALT1-associated cancer types disclosed in herein, comprising administering to the subject an effective amount of a compound of Formula (I), or a pharmaceutically acceptable salt thereof, or a pharmaceutical composition of QRQQcn / zznz / q / υιλι 139 this as defined herein. In some embodiments of any of the methods provided herein, a compound of Formula (I) is selected from Examples 1-211. Dysregulation of a MALT1 protease, a MALT1 gene, or the expression, activity or level of any (e.g., one or more) of these may contribute to tumorigenesis. For example, a fusion protein may have greater protease activity compared to a wild-type MALT1 protein; Increased expression (e.g., higher levels) of a wild-type MALT1 protease may occur in a mammalian cell due to abnormal cell signaling and / or deregulated autocrine / paracrine signaling (e.g., compared to a mammalian cell). non-cancerous control); MALT1 mRNA splice variants may also result in deregulation of MALT1. In some aspects, provided herein is a method of treating cancer in a subject in need thereof, including administering to the subject an effective amount of a compound of Formula (I), or a pharmaceutically acceptable salt. of this. Also provided herein is a method of treating a type of cancer associated with the CBM complex pathway (such as any of those disclosed herein) in a subject in need thereof, which includes administering to the subject an effective amount of a compound of Formula (I), or a pharmaceutically acceptable salt thereof. Also provided is a method of treating a type of cancer in a subject in need thereof, including (a) identifying the type of cancer as a type of cancer associated with the CBM complex pathway; and (b) administering to the subject an effective amount of a compound of Formula (I), or a pharmaceutically acceptable salt thereof. Identification of the type of cancer in the subject as a type of cancer associated with the CBM complex pathway can be performed by any suitable method. In some embodiments, the step of identifying the type of cancer in the subject as a type of cancer associated with the CBM complex pathway includes performing an assay to detect deregulation in a gene associated with the CBM complex pathway, a protein protease associated with the CBM complex pathway, or the expression, activity or level of any of these in a sample from the subject. In some embodiments, the method further includes obtaining a sample from the subject (e.g., a biopsy sample). An essay can be any appropriate essay. In some embodiments, the assay is selected from the group consisting of sequencing (e.g., pyrosequencing or next-generation sequencing), immunohistochemistry, enzyme-linked immunosorbent assay, and fluorescence in situ hybridization (FISH). Also provided herein is a method of treating a type of cancer in a subject in need thereof, which includes administering! subject an effective amount of a compound of Formula (I), or a pharmaceutically acceptable salt thereof, to a subject identified as having a type of cancer associated with the CBM complex pathway. Also provided herein is a method of treating a MALT1-associated cancer in a subject, including administering to a subject identified or diagnosed with a MALT1-associated cancer an effective amount of a compound of Formula (I). , or a pharmaceutically acceptable salt thereof. Also provided herein is a method of treating cancer in a subject in need thereof, which includes: (a) determining that the type of cancer is 140 associated with a deregulation of a MALT1 gene, a MALT1 protease, or the expression, activity or level of any of these; and (b) administering to the subject an effective amount of a compound of Formula (I), or a pharmaceutically acceptable salt thereof. The determination that the type of cancer is associated with a deregulation of a MALT1 gene, a MALT1 protease, or the expression, activity or level of any of these can be made by any appropriate method. In some embodiments, the step of determining that the type of cancer in the subject is a type of cancer associated with MALT1 includes performing an assay to detect deregulation in a MALT1 gene, a MALT1 protease protein, or the expression, activity or level of any of these in a sample of the subject. In some embodiments, the method further includes obtaining a sample from the subject (e.g., a biopsy sample). An essay can be any appropriate essay. In some embodiments, the assay is selected from the group consisting of sequencing (e.g., pyrosequencing or next-generation sequencing), immunohistochemistry, enzyme-linked immunosorbent assay, and fluorescence in situ hybridization (FISH). As described herein, a type of cancer associated with the CBM complex pathway may be any type of cancer associated with the appropriate CBM complex pathway (such as any of those described herein). In some embodiments, a type of cancer associated with the CBM complex pathway is selected from the group consisting of a type of cancer associated with the cell surface receptor of the CBM complex pathway, a type of cancer associated with a transducer signal between a cell surface receptor and a CBM complex, a component of a type of cancer associated with the CBM complex, a type of cancer associated with the MALT1 protease substrate, a type of cancer associated with a component of the NF-pathway κΒ downstream of a CBM complex, a type of cancer associated with a component of the JNK pathway downstream of a CBM complex, and a combination of these. In some embodiments, the type of cancer associated with the cell surface receptor of the CBM complex pathway is selected from the group consisting of a type of cancer associated with CD28, a type of cancer associated with BCR, a type of cancer HER1-associated, a type of HER2-associated cancer, and combinations of these. In some embodiments, the type of cancer associated with a signal transducer between a cell surface receptor and a CBM complex is a type of cancer associated with protein kinase C beta (PKCP), a type of cancer associated with protein kinase C theta (PCK0) or a combination of these. In some embodiments, the component of a type of cancer associated with the CBM complex is selected from the group consisting of a type of cancer associated with MALT1, a type of cancer associated with CARD11, a type of cancer associated with CARD14, a type of CARD10-associated cancer, a type of CARD9-associated cancer, a type of BCL10-associated cancer and combinations of these. In some embodiments, the component of a cancer type associated with the CBM complex is selected from the group consisting of a cancer type associated with MALT1, a cancer type associated with CARD11, a cancer type associated with BCL10 and combinations of these. See, for example, Tables Β1, B2 and B3 for example deregulations in MALT1, CARD11 and BCL10. In some embodiments, the type of cancer associated with the MALT1 protease substrate is selected from the group consisting of a type of cancer associated with BCL10, a type of cancer associated with A20, a type of cancer associated with CYLD, a type of RelB-associated cancer, a type of cancer associated with regnase-1, a type of cancer associated with roquine-1, a type of cancer associated with HOIL1, a type of 141 NIK-associated cancer, a type of LIMAIa-associated cancer and a combination of these. In some embodiments, the MALT1 protease substrate-associated cancer type is selected from the group consisting of a BCL10-associated cancer type, an A20-associated cancer type, a CYLD-associated cancer type, and combinations of these. . See, for example, Tables B3 and B4 for example deregulations in BCL10 and A20. In some embodiments, the type of cancer associated with a component of the NF-κΒ pathway downstream of a CBM complex is selected from the group consisting of a type of cancer associated with TAK1, a type of cancer associated with TRAF6, a type of cancer associated with TAB1, type of cancer associated with TAB2, type of cancer associated with TAB3, type of cancer associated with MKK7, type of cancer associated with IKKa, type of cancer associated with ΙΚΚβ, type of IKKy-associated cancer, an IkBa-associated cancer, a p50-associated cancer, a p65 (RelA)-associated cancer, a c-Rel-associated cancer, and combinations thereof. In some embodiments, the cancer type associated with a component of the NF-κΒ pathway downstream of a CBM complex is an IKKy-associated cancer type. In some embodiments, the type of cancer associated with a component of the JNK pathway downstream of a CBM complex is selected from the group consisting of a type of cancer associated with JNK1, a type of cancer associated with JNK2, a type of JNK3-associated cancer, a MYD88 transcription factor-associated cancer, an AP-1 transcription factor-associated cancer, and combinations thereof. In some embodiments, the type of cancer associated with the CBM complex pathway is a type of cancer associated with MALT1. A type of MALT1-associated cancer may have any suitable dysregulation, such as any of those described herein. In some embodiments, the MALT1-associated cancer type comprises an IAP2-MALT1 fusion. In some embodiments, the MALT 1-associated cancer type comprises an IGH-MALT1 fusion. Also provided herein are methods for treating diseases or disorders, autoimmune disorders and inflammatory disorders associated with the CBM complex pathway. Accordingly, provided herein is a method of treating an autoimmune disorder in a subject in need thereof, which includes administering to the subject an effective amount of a compound of Formula (I), or a pharmaceutically acceptable salt. of this. Also provided herein is a method of treating a MALT1-associated autoimmune disorder in a subject, including administering to a subject identified or diagnosed with a MALT1-associated autoimmune disorder an effective amount of a compound of Formula (I), or a pharmaceutically acceptable salt of this. In some cases, a method of treating an autoimmune disorder in a subject in need thereof is provided herein, including: (a) determining that the autoimmune disorder is associated with a deregulation of a MALT1 gene, a MALT1 protease, or the expression, activity or level of any of these; and (b) administering to the subject an effective amount of a compound of Formula (I), or a pharmaceutically acceptable salt thereof. Also provided herein is a method of treating a MALT 1-associated autoimmune disorder in a subject, which includes administering an effective amount of a compound of Formula (I), or a pharmaceutically acceptable salt thereof to a subject who was determined to have a MALT1-associated autoimmune disorder. Furthermore, provided herein is a method of treating an inflammatory disorder in a subject in need thereof, which 142 includes administering to the subject an effective amount of a compound of Formula (I), or a pharmaceutically acceptable salt thereof. In some cases, a method of treating a MALT1-associated inflammatory disorder in a subject is provided herein, including administering to a subject identified or diagnosed with a MALT1-associated inflammatory disorder an effective amount of a compound of Formula (I ), or a pharmaceutically acceptable salt thereof. Also provided herein is a method of treating an inflammatory disorder in a subject in need thereof, including: (a) determining that the inflammatory disorder is associated with a deregulation of a MALT1 gene, a MALT1 protease, or the expression, activity or level of any of these; and (b) administering to the subject an effective amount of a compound of Formula (I), or a pharmaceutically acceptable salt thereof. Also provided herein is a method of treating a MALT1-associated inflammatory disorder in a subject, including administering an effective amount of a compound of Formula (I), or a pharmaceutically acceptable salt thereof to a subject. subject who was determined to have an inflammatory disorder associated with MALTI. Furthermore, provided herein is a method of treating a disease or disorder associated with the CBM complex pathway in a subject in need thereof, which includes administering to the subject an effective amount of a compound of Formula (I), or a pharmaceutically acceptable salt of this. Also provided is a method of treating a disease or disorder in a subject in need thereof, including: (a) identifying the type of cancer as a disease or disorder associated with the CBM complex pathway; and (b) administering to the subject an effective amount of a compound of Formula (I), or a pharmaceutically acceptable salt thereof. Furthermore, provided herein is a method of treating a disease or disorder in a subject in need thereof, which includes: administering to the subject an effective amount of a compound of Formula (I), or an acceptable salt from the point of pharmaceutical view of this to a subject in whom a disease or disorder associated with the CBM complex pathway was identified. A disease or disorder associated with the CBM complex pathway may be any suitable CBM complex pathway associated disease or disorder, such as any of those described herein. In some embodiments, the disease or disorder associated with the CBM complex pathway is an autoimmune disease. In some embodiments, the disease or disorder associated with the CBM complex pathway is an inflammatory disease. In some embodiments, the type of cancer associated with the CBM complex pathway is selected from the group consisting of a type of cancer associated with the cell surface receptor of the CBM complex pathway, a disease or a disorder associated with a signal transducer between a cell surface receptor and a CBM complex, a component of a type of cancer associated with the CBM complex, a type of cancer associated with the MALT1 protease substrate, a disease or disorder associated with a component of the pathway NF-κΒ downstream of a CBM complex, a disease or disorder associated with a component of the JNK pathway downstream of a CBM complex, and a combination thereof. In some embodiments, the disease or disorder associated with the CBM complex pathway is a disease or disorder associated with MALT 1. In some cases, the compounds of Formula (I), or a pharmaceutically acceptable salt thereof, may be useful for inhibiting cell processes, such as inhibiting cell proliferation. Consequently, it 143 provides herein a method for inhibiting the proliferation of mammalian cells, which includes contacting the mammalian cell with a compound of Formula (I), or a pharmaceutically acceptable salt thereof. Also provided herein is a method of inhibiting the activity of the CBM complex pathway in a mammalian cell, which includes contacting the mammalian cell with a compound of Formula (I), or a commercially acceptable salt. from a pharmaceutical point of view of this. Also provided herein is a method of inhibiting the activity of the MALT1 protease in a mammalian cell, which includes contacting the mammalian cell with a compound of Formula (I), or a technically acceptable salt. pharmacist of this. In some embodiments, contacting occurs in vivo. In some embodiments, contacting occurs in vitro. A mammalian cell can be any suitable cell. In some embodiments, the mammalian cell is a mammalian immune cell. In some embodiments, the mammalian cell is a mammalian cancer cell. In some embodiments, the mammalian cancer cell is a cancer cell associated with the mammalian CMB complex pathway. In some embodiments, the mammalian cancer cell is a mammalian MALT1-associated cancer cell. In some embodiments, the mammalian cell has deregulation of a MALT1 gene, a MALT1 protease protein, or the expression, activity or level of any of these. In some embodiments, the deregulation of a MALT1 gene, a MALT1 protease protein, or the expression, activity or level of any of these is an IAP2-MALT1 fusion, an IGH-MALT1 fusion, or a combination of these. The compounds of Formula (I), or a pharmaceutically acceptable salt thereof, may also be useful in the manufacture of medicaments. Accordingly, provided herein is a use of a compound of Formula (I), or a pharmaceutically acceptable salt thereof, in the manufacture of a medicament for the treatment of a disease or disorder associated with the CBM complex pathway. A disease or disorder associated with the CBM complex pathway may be any disease or disorder associated with the appropriate CBM complex pathway, such as those described herein. In some embodiments, the disease or disorder associated with the CBM complex pathway is selected from the group consisting of a type of cancer associated with the cell surface receptor of the CBM complex pathway, a disease or disorder associated with a signal transducer between a cell surface receptor and a CBM complex, a component of a type of cancer associated with the CBM complex, a type of cancer associated with the MALT1 protease substrate, a disease or disorder associated with a component of the NF-κΒ pathway downstream of a CBM complex, a disease or disorder associated with a component of the JNK pathway downstream of a CBM complex, and a combination of these. In some embodiments, the disease or disorder associated with the CBM complex pathway is an autoimmune disorder associated with the CBM complex pathway. In some embodiments, the disease or disorder associated with the CBM complex pathway is an inflammatory disorder associated with the CBM complex pathway. In some embodiments, the CBM complex pathway-associated disease or disorder is a type of CBM complex pathway-associated cancer. In some embodiments, the disease or disorder associated with the CBM complex pathway is a disease or disorder associated with MALT1. In some embodiments, the MALT1-associated disease or disorder comprises a deregulation of a MALT1 gene, a MALT1 protease protein, or the expression, activity or level of any of these. In some embodiments, QRFQCn / ZZnZ / q / ΥΙΛΙ 144 deregulation of a MALT1 gene, a MALT1 protease protein, or the expression, activity or level of any of these is an IAP2-MALT1 fusion, an IGH-MALT1 fusion, or a combination of these. In some embodiments, the compounds provided herein exhibit penetration into the brain and / or the central nervous system (CNS). Such compounds are capable of crossing the blood-brain barrier and inhibiting a MALT1 protease in the brain and / or other CNS structures. In some embodiments, the compounds provided herein are capable of crossing the blood-brain barrier in an effective amount. For example, treatment of a subject with cancer (e.g., a type of MALT1-associated cancer, such as a type of MALT 1-associated brain or CNS cancer) may include administration (e.g., oral administration) of the composed to the subject. In some such embodiments, the compounds provided herein are useful for treating a primary brain tumor or a metastatic brain tumor. For example, the compounds can be used in the treatment of one or more gliomas such as glioblastoma (also called glioblastoma multiforme), astrocytomas, oligodendrogliomas, ependymomas and mixed gliomas, meningiomas, medulloblastomas, gangliogliomas, schwannomas (neurilemmomas) and craniopharyngiomas (see, for example, For example, the tumors listed in Louis, D.N. et al. Acta Neuropathol 131(6), 803-820 (June 2016)). In some embodiments, the brain tumor is a primary brain tumor. In some embodiments, the subject is pretreated with another antineoplastic agent, for example, another protease inhibitor (for example, a compound that is not a compound of Formula (I)). In some embodiments, the brain tumor is a metastatic brain tumor. In some embodiments, the subject is pretreated with another antineoplastic agent, for example, another protease inhibitor (for example, a compound that is not a compound of Formula (I)). In some embodiments of any of the methods or uses described herein, an assay used to determine whether the subject has a deregulation of a gene (e.g., a MALT1 gene) or a protein (e.g., a MALT1 protein) , or the expression, activity or level of any of these, using a sample from a subject may include, for example, next generation sequencing, immunohistochemistry, fluorescence microscopy, FISH separation analysis, Southern blotting, Western blotting, FACS analysis, Northern blotting and PCR-based amplification (e.g. RT-PCR and quantitative real-time RT-PCR). As is known in the art, assays are typically performed, for example, with at least one labeled nucleic acid probe or at least one labeled antibody or antigen-binding fragment thereof. The assays may use other detection methods known in the art to detect deregulation of a gene (e.g., a MALT1 gene), a protein (e.g., a MALT1 protein), or the expression, activity or levels of any of these. . In some embodiments, the sample is a biological sample or a biopsy sample (e.g., a paraffin-embedded biopsy sample) from the subject. In some embodiments, the subject is a subject believed to have a MALT1-associated cancer, a subject who has one or more symptoms of a MALT1-associated cancer, and / or a subject who has an increased risk. of developing a type of cancer associated with MALT 1. In some embodiments, dysregulation of a gene (e.g., a MALT1 gene), a MALT1 protein (e.g., a MALT1 protein), or the expression, activity or level of any of these can be identified with a biopsy. QRFQCn / ZZnZ / q / ΥΙΛΙ 145 liquid (variously called fluid biopsy or fluid phase biopsy). Liquid biopsy methods can be used to detect total tumor burden and / or deregulation of a gene (e.g., a MALT1 gene), a MALT1 protein (e.g., a MALT1 protein), or the expression, activity or level of any of these. Liquid biopsies can be performed on biological samples obtained relatively easily from a subject (for example, through a simple blood draw) and are generally less invasive than traditional methods used to detect tumor burden and / or gene deregulation ( for example, a MALT1 gene), a protein (for example, a MALT1 protein), or the expression, activity or level of any of these. In some embodiments, liquid biopsies can be used to detect the presence of dysregulation of a gene (e.g., a MALT1 gene), a protein (e.g., a MALT1 protein), or the expression, activity or level of any of these at an earlier stage than traditional methods. In some embodiments, the biological sample to be used in a liquid biopsy may include blood, plasma, urine, cerebrospinal fluid, saliva, sputum, bronchoalveolar lavage, bile, lymphatic fluid, cystic fluid, feces, ascites, and combinations of these. In some embodiments, a liquid biopsy can be used to detect circulating tumor cells (CTCs). In some embodiments, a liquid biopsy can be used to detect cell-free DNA. In some embodiments, the cell-free DNA detected with a liquid biopsy is circulating tumor DNA (ctDNA) that is derived from tumor cells. ctDNA analysis (e.g., using sensitive detection techniques such as, but not limited to, next-generation sequencing (NGS), traditional POR, digital PCR, or microarray analysis) can be used to identify deregulation of a gene (e.g. , a MALT1 gene), a protein (for example, a MALT1 protein), or the expression, activity or level of any of these. In some embodiments, ctDNA derived from a single gene can be detected with a liquid biopsy. In some embodiments, ctDNA derived from a plurality of genes can be detected (e.g., 2, 3,4, 5,6, 7,8,9, 10,15,20,25, 30,35,40 ,45, 50, 55,60, 65,70,75,80, 85,90, 95,100 or more, or any number of genes between these numbers) with a liquid biopsy. In some embodiments, ctDNA derived from a plurality of genes can be detected with any of a variety of commercially available test panels (e.g., commercially available test panels designed to detect deregulation of a gene ( for example, a MALT1 gene), a protein (for example, a MALT1 protein), or the expression, activity or level of any of these). Liquid biopsies can be used to detect dysregulation of a gene (e.g., a MALT1 gene), a protein (e.g., a MALT1 protein), or the expression, activity, or level of any of these, including, but not limited to, mutations. point or single nucleotide variants (SNVs), copy number variants (CNVs), genetic fusions (e.g., translocations or rearrangements), insertions, deletions, or any combination of these. In some embodiments, a liquid biopsy can be used to detect a germline mutation. In some embodiments, a liquid biopsy can be used to detect a somatic mutation. In some embodiments, a liquid biopsy can be used to detect a primary genetic mutation (e.g., a primary mutation or primary fusion that is associated with the initial development of a disease, e.g., cancer). In some embodiments, a dysregulation of a gene (e.g., a MALT1 gene), a protein (e.g., a MALT1 protein), or the expression, activity or level of any of these identified with a liquid biopsy is also present. QAFQCn / ZZnZ / q / ΥΙΛΙ 146 in a cancer cell that is present in the subject (for example, in a tumor). In some embodiments, any type of deregulation of a gene (e.g., a MALT1 gene), a protein (e.g., a MALT1 protein), or the expression, activity or level of any of these described herein can be detected with a liquid biopsy. In some embodiments, a genetic mutation identified by a liquid biopsy may be used to identify the subject as a candidate for a particular treatment. For example, detection of dysregulation of a gene (e.g., a MALT1 gene), a protein (e.g., a MALT1 protein), or the expression, activity or level of any of these in the subject may indicate that the subject will respond to a treatment that includes the administration of a compound of Formula (I), or a pharmaceutically acceptable salt thereof. Liquid biopsies may be performed at multiple time points during a diagnostic cycle, a monitoring cycle, and / or a treatment cycle to determine one or more clinically relevant parameters, including, but not limited to, disease progression and / or efficacy. of a treatment. For example, a first liquid biopsy may be performed at a first time point and a second liquid biopsy may be performed at a second time point during a diagnostic cycle, a monitoring cycle, and / or a treatment cycle. In some embodiments, the first time point may be a time point prior to the diagnosis of a disease in a subject (e.g., when the subject is healthy), and the second time point may be a time point after the development of the disease. disease in the subject (for example, the second time point can be used to diagnose the subject with the disease). In some embodiments, the first time point may be a time point prior to the diagnosis of a disease in a subject (e.g., when the subject is healthy), after which the subject is monitored, and the second time point may be a time point after monitoring the subject. In some embodiments, the first time point may be a time point after a disease is diagnosed in a subject, after which a treatment is administered to the subject, and the second time point may be a time point after the administration of the treatment; In such cases, the second time point can be used to evaluate the effectiveness of the treatment (for example, whether the gene mutations detected at the first time point are reduced in abundance or are undetectable). In some embodiments, a treatment to be administered to a subject may include a compound of Formula (I), or a pharmaceutically acceptable salt thereof. In some embodiments, the efficacy of a compound of Formula (I), or a pharmaceutically acceptable salt thereof, can be determined by evaluating the allelic frequency of a deregulation of a gene (e.g., a MALT1 gene) in cfDNA obtained from a subject at different time points, for example, cfDNA obtained from the subject at a first time point and cfDNA obtained from the subject at a second time point, where at least one dose of a compound of Formula (I ), or a pharmaceutically acceptable salt thereof, is administered to the subject between the first and second time points. Some embodiments of these methods may further include administering to the subject at least one dose of the compound of Formula (I), or a pharmaceutically acceptable salt thereof, between the first and second time points. For example, a reduction (for example, a reduction from 1% to about 99%, a reduction from 1% to about 95%, a reduction from 1% to about 90%, a reduction from 1% to about 85%, a reduction of 1% to around 80%, a reduction of 1% to around 147%, a reduction of 1% to about 70%, a reduction of 1% to about 65%, a reduction of 1% to about 60%, a reduction of 1% to about 55%, a reduction of 1% to about 50%, a reduction of 1% to about 45%, a reduction of 1% to about 40%, a reduction of 1% to about 35%, a reduction of 1% to about 30 %, a reduction of 1% to about 25%, a reduction of 1% to about 20%, a reduction of 1% to about 15%, a reduction of 1% to about 10%, a reduction of 1 % to about 5%, a reduction of about 5% to about 99%, a reduction of about 10% to about 99%, a reduction of about 15% to about 99%, a reduction of about from 20% to about, a reduction of about 25% to about 99%, a reduction of about 30% to about 99%, a reduction of about 35% to about 99%, a reduction of about 40% to about 99%, a reduction of about 45% to about 99%, a reduction of about 50% to about 99%, a reduction of about 55% to about 99%, a reduction from about 60% to about 99%, a reduction from about 65% to about 99%, a reduction from about 70% to about 99%, a reduction from about 75% to about 95% , a reduction of about 80% to about 99%, a reduction of about 90% to about 99%, a reduction of about 5% to about 10%, a reduction of about 10% to about 30%, a reduction of about 25% to about 50%, a reduction of about 40% to about 60%, a reduction of about 95% to about 99%, a reduction of about 5% to about 25%, a reduction of about 20% to about 40%, a reduction of about 35% to about 55%, a reduction of about 50% to about 75%, a reduction of about 60% % to about 80% or a reduction from about 65% to about 85%) of the allele frequency (AF) of the deregulation of a gene (e.g., MALT1 gene) in the cfDNA obtained from the subject in the second point temporal comparison with the allele frequency (AF) of the deregulation of a gene (e.g., MALT1 gene) in the cfDNA obtained from the subject at the first time point indicates that the compound of Formula (I), or an acceptable salt from the pharmaceutical point of view of this, was effective in the subject. In some embodiments, the AF is reduced so that the level is below the detection limit of the instrument. Alternatively, an increase in the allele frequency (AF) of the deregulation of a gene (e.g., MALT1 gene) in the cfDNA obtained from the subject at the second time point compared to the allele frequency (AF) of the deregulation of a gene (e.g., MALT1 gene) in the cfDNA obtained from the subject at the first time point indicates that the compound of Formula (I), or a pharmaceutically acceptable salt thereof, was not effective in the subject . Some embodiments of these methods may further include administering additional doses of a compound of Formula (I), or a pharmaceutically acceptable salt thereof, to a subject in whom a compound of Formula (I) was determined to be Formula (I), or a pharmaceutically acceptable salt thereof, was effective. Some embodiments of these methods may further include administering a different treatment (for example, a treatment that does not include the administration of a compound of Formula (I), or a pharmaceutically acceptable salt thereof, as monotherapy ) to a subject in which a compound of Formula (I), or a pharmaceutically acceptable salt thereof, was determined to be ineffective. 148 In some examples of these methods, the time difference between the first and second time points can be from about 1 day to about 1 year, from about 1 day to about 11 months, from about 1 day to about from 10 months, from about 1 day to about 9 months, from about 1 day to about 8 months, from about 1 day to about 7 months, from about 1 day to about 6 months, from about from 1 day to about 5 months, from about 1 day to about 4 months, from about 1 day to about 3 months, from about 1 day to about 10 weeks, from about 1 day to about 2 months, about 1 day to about 6 weeks, about 1 day to about 1 month, about 1 day to about 25 days, about 1 day to about 20 days, about 1 day to about 15 days, about 1 day to about 10 days, about 1 day to about 5 days, about 2 days to about 1 year, about 5 days to about 1 year, about 10 days to about 1 year, about 15 days to about 1 year, about 20 days to about 1 year, about 25 days to about 1 year, about 1 month to about 1 year, about 6 weeks to about 1 year, about 2 months to about 1 year, about 3 months to about 1 year, about 4 months to about 1 year , about 5 months to about 1 year, about 6 months to about 1 year, about 7 months to about 1 year, about 8 months to about 1 year, about 9 months to about 1 year, from about 10 months to about 1 year, from about 11 months to about 1 year, from about 1 day to about 7 days, from about 1 day to about 14 days, from about 5 days to about 10 days, from about 5 days to about 20 days, from about 10 days to about 20 days, from about 15 days to about 1 month, from about 15 days to about 2 months, about 1 week to about 1 month, about 2 weeks to about 1 month, about 1 month to about 3 months, about 3 months to about 6 months, about 4 months to about 6 months, about 5 months to about 8 months or about 7 months to about 9 months. In some embodiments of these methods, the subject may be pre-detected as having a type of cancer that has a deregulated gene (e.g., any of the examples of a deregulated gene described herein) (e.g., a MALT1 gene). ). In some embodiments of these methods, a subject may have been previously diagnosed with any of the types of cancer described herein. In some embodiments of these methods, the subject may have one or more metastases (e.g., one or more brain metastases). In some of the above embodiments, the cfDNA comprises ctDNA, such as ctDNA associated with MALT1. For example, cfDNA is ctDNA, such as ctDNA associated with MALT1. In some embodiments, at least a portion of the cfDNA is determined to be MALT1-associated ctDNA, for example, a sequenced and / or quantified amount of the total cfDNA is determined to have a MALT1 fusion and / or MALT1 overexpression. In the field of medical oncology, it is normal practice to use a combination of different forms of treatment to treat each subject with cancer. In medical oncology, the other components of such treatment or co-therapy, in addition to the compositions provided herein, may be, for example, surgery, radiotherapy and chemotherapeutic agents, such as other protease inhibitors, kinase inhibitors, transduction inhibitors. signal and / or monoclonal antibodies. 149 For example, a surgery may be open surgery or minimally invasive surgery. The compounds of Formula (I), or a pharmaceutically acceptable salt thereof, may therefore also be useful as adjuvants for cancer treatment, that is, they may be used in combination with one or more treatments or additional therapeutic agents, for example, a chemotherapeutic agent that acts through the same or a different mechanism of action. In some embodiments, a compound of Formula (I), or a pharmaceutically acceptable salt thereof, may be used prior to administration of an additional therapeutic agent or additional treatment. For example, a subject in need may be administered one or more doses of a compound of Formula (I), or a pharmaceutically acceptable salt thereof, over a period of time and then the subject may undergo at least partial resection of the tumor. In some embodiments, treatment with one or more doses of a compound of Formula (I), or a pharmaceutically acceptable salt thereof, reduces tumor size (e.g., tumor burden) before of at least partial resection of the tumor. In some embodiments, a subject in need may be administered one or more doses of a compound of Formula (I), or a pharmaceutically acceptable salt thereof, over a period of time and with one or more rounds of radiotherapy. In some embodiments, treatment with one or more doses of a compound of Formula (I), or a pharmaceutically acceptable salt thereof, reduces tumor size (e.g., tumor burden) prior to the one or more rounds of radiotherapy. . In some embodiments, a subject has a type of cancer (e.g., a locally advanced or metastatic tumor) that is resistant or intolerant to standard treatment (e.g., administration of a chemotherapeutic agent), such as a first inhibitor. MALT 1, a kinase inhibitor, immunotherapy, cellular or genetic treatment, or radiation (such as radioactive iodine). In some embodiments, a subject has a type of cancer (e.g., a locally advanced or metastatic tumor) that is resistant or intolerant to prior treatment (e.g., administration of a chemotherapeutic agent, such as a first MALT1 inhibitor). or other protease inhibitor, immunotherapy, cellular or genetic treatment, or radiation (for example, radioactive iodine). In some embodiments, a subject has a type of cancer (e.g., a locally advanced or metastatic tumor) that does not have a standard treatment. In some embodiments, a subject was naïve to MALT1 protease inhibitor treatment. For example, the subject was not treated with a selective MALT1 protease inhibitor. In some embodiments, a subject has already received prior treatment with MALT1 protease inhibitor. In some embodiments of any of the methods described herein, the compound of Formula (I), or a pharmaceutically acceptable salt thereof, is administered in combination with an effective amount of at least one agent. additional therapeutic selected from one or more additional treatments or therapeutic agents (for example, chemotherapeutics or immunomodulators). An additional treatment or therapeutic agent may be any appropriate additional treatment or therapeutic agent, such as any of those described herein. Non-limiting examples of additional therapeutic agents include: other therapeutic agents targeting MALT1 (i.e., a first or second MALT1 protease inhibitor, e.g., JNJ-67856633 or CTX-177), other protease inhibitors, kinase inhibitors ( for example, therapeutic agents targeting receptor tyrosine kinase, such as QRQQcn / zznz / q / υιλι 150 BTK or EGFR inhibitors), signal transduction pathway inhibitors, checkpoint inhibitors, apoptosis pathway modulators (for example, venetoclax or obataclax); cytotoxic chemotherapeutic agents, treatments targeting angiogenesis, agents targeting the immune system (including antibody- and cell-based immunotherapies and antibody-drug conjugates), and radiotherapy. In some embodiments, the compound of Formula (I), or a pharmaceutically acceptable salt thereof, and the additional therapeutic agent are administered simultaneously as separate doses. In some embodiments, the compound of Formula (I), or a pharmaceutically acceptable salt thereof, and the additional therapeutic agent are administered as separate doses sequentially in any order. In some embodiments, the other therapeutic agent targeting MALT1 is another protease inhibitor that exhibits MALT 1 inhibitory activity. In some embodiments, the other therapeutic agent targeting MALT 1 is selective for a MALT1 protease. Exemplary MALT1 protease inhibitors may exhibit an inhibition activity (IC50) against a MALT 1 protease of less than about 1000 nM, less than about 500 nM, less than about 200 nM, less than about 100 nM. , less than about 50 nM, less than about 25 nM, less than about 10 nM or less than about 1 nM, as measured in an assay described herein. In some embodiments, a MALT1 protease inhibitor may exhibit inhibition activity (IC50) against a MALT1 protease of less than about 25 nM, less than about 10 nM, less than about 5 nM, or less than about 1 nM, as measured in an assay as provided herein. Non-limiting examples of protease-targeting therapeutic agents (e.g., a first MALT1 inhibitor or a second MALT1 inhibitor) include JNJ-67856633 and CTX-177. Non-limiting examples of multi-kinase inhibitors include alectinib (9-ethyl-6,6-dimethyl-8-[4-(morpholin-4¡l)piperid¡n-1-¡l]-11-oxo-6.11- dihydro-5H-benzo[b]carbazole-3-carbonitrile); amuvatinib (MP470, HPK56) (N-(1,3benzodioxol-5-ylmethyl)-4-([1]benzofuro[3,2-d]pririm¡din-4-yl)piperazin-1-carbot oam!da); apatinib (YN968D1) (N-[4-(1-cyanocyclopentyl)phenyl-2-(4-picolyl)amino-3-nicotinamide methanesulfonate); cabozantinib (Cometriq XL-184) (N(4-((6,7-dimethoxyquinol¡n-4-¡l)ox¡)phenyl)-N”-(4-fluorophen¡l)cyclopropane-1 ,1-dicarboxamide); dovitinib (TKI258; GFKI-258; CHIR-258) ((3Z)-4-amino-5-fluoro-3-[5-(4-methylpiperazin-1-yl)-1,3-dihydrobenzimidazol-2-ylidene] qu¡nol¡n-2-one); famitinib (5-[2-(diethylamino)ethyl]-2-[(Z)-(5-fluoro-2-oxo-1 H-indol-3-ylidene)methyl]-3-methyl-6,7-d hydro-1 H-pyrrolo[3,2-c]pyridín-4-one); fedratinib (SAR302503, TG101348) (N-(2-methyl-2-propanyl)-3-{[5-met¡l-2-({4-[2-(1 -pyrrolíd¡n¡l)ethox ¡]phenyl}amino)-4pyrimidinyl]amino}benzenesulfonamide); foretinib (XL880, EXEL-2880, GSK1363089, GSK089) (N1”-[3-fluoro-4-[[6-methoxy¡7-(3-morpholinopropoxy)-4-quinolyl]oxy]phenyl]-N1 - (4-fluorophenyl)cyclopropane-1,1-dicarboxamide); fostamantinib (R788) (2Hpyrido[3,2-b]-1,4-oxazin-3(4H)-one, 6-[[5-fluoro-2-[(3,4,5-trimethoxifen ¡l)amino]-4-pyrim¡d¡n¡l]amino]-2,2-dimethyl-4[(phosphonooxy)methyl]-, sodium salt (1:2)); ilorasertib (ABT-348) (1 -(4-(4-amino-7-(1 -(2-hydroxyethyl)-1 H-pyrazol-4-yl)thieno[3,2c]pyridin-3-yl)phen l)-3-(3-fluorophenyl)urea); lenvatinib (E7080, Lenvima) (4-[3-chloro-4-(cycloprop¡laminocarbonyl)aminophenoxy¡]7-methoxy-6-quinolinecarboxamide); motesanib (AMG 706) (N-(3,3-dimethyl-2,3-dihydro-1H-indol-6-yl)-2-[(pyridin-4ylmethyl)amino]pyridine-3 -carboxamide); nintedanib (3-Z-[1-(4-(N-((4-methyl-piperazin-1-yl)-methylcarbonyl)-N-methyl-amino)anilino)-1-phenyl-methylene]-6-methioxycarbonyl -2-indolinone); ponatinib (AP24534) (3-(2-midazo[1,2-b]pyridazin-3-ilethynyl)-4 151 methyl-N-[4-[(4-methyl!perazin-1-yl)methyl]-3-(trifluoromethyl)phenyl]benzamide); PP242 (torkinib) (2-[4-amino-1-(1-methylethyl)-1 Hp¡razolo[3,4-d]pyrimidín-3-¡l]-1 H-indole-5- ol); quizartinib (1-(5-(tert-butyl)isoxazol-3-íl)-3-(4-(7-(2morpholinoethoxy)benzo[d]imídazo[2,1 -b]thiazol-2-yl )phenyl)urea); regorafenib (BAY 73-4506, stivarga) (4-[4-({[4-chloro3-(tnfluoromethyl)phenyl]carbamo¡l}amino)-3-fluorophenoxy¡]-N-hydrate meth¡lp¡r¡dina-2-carboxamide); RXDX-105 (CEP-32496, agerafenib) (1 -(3-((6,7-dimethoxyquinazolin-4-yl)oxy)phenyl)-3-(5-(1,1,1-trifluoro-2-methylpropan -2-yl)isoxazol-3-yl)urea); semaxanib (SU5416) ((3Z)-3-[(3,5-dimethyl-1H-pyrrole-2-¡l)methyladene]-1,3-dihydro-2H -ndol-2-one); sitravatinib (MGCD516, MG516) (N-(3-fluoro-4-{[2-(5-{[(2-methox¡ethyl)amino]methyl}-2-pyridin¡l)t (eno[3,2-b]pyridn-7-yl]oxyphenyl)-N'-(4-fluorophenyl)-1,1 cyclopropanedicarboxamide); sorafenib (BAY 43-9006) (4-[4-[[[[4-chloro-3-(trifluoromethyl)phenyl]amino]carbonyl]amino]phenoxy¡]N-methyl -2-pyridinecarboxannide); vandetanib (N-(4-bromo-2-fluorophenyl)-6-methoxy¡-7-[(1 -methylpiper¡din-4-¡l)methoxy¡]quinazolin4-amine); vatalanib (PTK787, PTK / ZK, ZK222584) (N-(4-chlorophenyl)-4-(pyridin-4-ylmethyl)phthalazine-1-amine); AD-57 (N-[4-[4amino-1-(1-methylethyl)-1 H-prázolo[3,4-d]pyrim¡din-3-¡l]phen¡l]-N'- [3-(trifluoromethyl)phenyl]-urea); AD-80 (1-[4-(4-amino-1-propan2-¡lp¡razolo[3,4-d]p¡r¡m¡d¡n-3-¡l)phen¡l]-3 -[2-fluoro-5-(trifluoromethyl)phenyl]urea); AD-81 (1-(4-(4-amino-1-isoprop¡l-1 Hp¡razolo[3,4-d]pyrimidin-3-yl)phen¡l)-3-(4 -chloro-3-(trifluoromethyl)phenyl)urea); ALW-ll-41-27 (N-(5-((4-((4-ethylpiperaz¡n-1-yl)methyl)3-(trifluoromethyl)phen¡l)carbamol) -2-met¡lfen¡l)-5-(t¡ofen-2-¡l)nicot¡nam¡da); BPR1K871 (1-(3-chlorophenyl)-3-(5-(2-((7-(3(dimethylamino)propoxy¡)quinazolin-4-¡l)amino)et l)thiazol-2-l)urea); CLM3 (1-phenethyl-N-(1-phenylethyl)-1 H-pyrazolo[3,4-d]pyrimidín4-amine); EBI-907 (N-(2-chloro-3-(1-cyclopropyl-8-methoxy-3H-pyrazol[3,4-c]soquinolin-7-l)4- fluorophenyl)-3-fluoropropane-1sulfonamide); NVP-AST-487 (N-[4-[(4-ethyl-1-piperazin¡l)methyl]-3-(trifluoromethyl)phen¡l]-N'-[4-[[ 6-(methylamino)-4pyrimidynyl]oxy]phenyl]-urea); NVP-BBT594 (BBT594) (5-((6-acetamidop¡r¡m¡d¡n-4-¡l)oxy)-N-(4-((4-methylp¡perazin-1-yl)methyl) -3(trifluoromethyl)phenyl)indoly n-1-carboxamide); PD173955 (6-(2,6-dichlorophenyl)-8-methyl-2-(3-methi Isulfanila n ylino)pyrido[2,3d]pyrimidin-7-one); PP2 (4-amino-5-(4-chlorophenyl)-7-(dimethylethyl)pyrazolo[3,4-d]pyrimidine); PZ-1 (N-(5-(tert-butyl)isoxazol-3¡l)-2-(4-(5-(1-methyl-1H-pyrazol-4-yl)-1Hbenzo[d ]¡m¡dazol-1-¡l)phen¡l)acetam¡de); RPI-1 (1,3-dihydro-5,6-dimethoxy¡-3-[(4hydroxyphenyl)methylene]-H-indol-2-one; (3E)-3-[(4-hydroxyphenyl)methylidene ]-5,6-dimethoxy-1 H-indol-2-one); SGI-7079 (3-[2-[[3fluoro-4-(4-methyl-1-p¡perazinyl)phenyl]amino]-5-methyl-7H-pyrrolo[2,3-d]pyrimidin -4-yl]-benzenacetonitrile); SPP86 (1-isopropyl-3(phenylethynyl)-l H-pyrazolo[3,4-d]pyrimidin-4-amine); SU4984 (4-[4-[(E)-(2-oxo-1 H-indol-3-ylidene)methyl]phenyl]piperazin-1carbaldehyde); sunitinb (SU11248) (N-(2-diethylaminoethyl)-5-[(Z)-(5-fluoro-2-oxo-1 H-indol-3-yl¡dene)methyl]-2,4-dimethyl -1Hyrrolo-3-carboxamide); TG101209 (N-tert-butyl-3-(5-methyl-2-(4-(4-methylpiperazin-1-yl)phenylamino)pyrimidin-4-lamino)benzenesulfonamide); witaferin A ((43,53,6p.22R)-4.27-dihdroxy-5,6:22.26-diepoxyergosta-2.24-diene-1.26dione); XL-999 ((Z)-5-((1-ethyllipíperidín-4-íl)amino)-3-((3-fluorophenyl)(5-methyl-1 H-imidazole- 2-yl)methylene)indolin-2-one); BPR1J373 (a 5-phen¡lt¡azol-2-ilamin-pyrmidine derivative); CG-806 (CG'806); DCC-2157; GTX-186; HG-6-63-01 ((E)-3(2-(4-chloro-1 H-pyrrolo[2,3-b]pind¡n-5-yl)vin¡l)-N-( 4-((4-ethylpiperazin-1-yl)methyl)-3-(trifluoromethyl)phenyl)-4-methylbenzamide); SW01 (cyclobenzaprine hydrochloride); XMD 15-44 (generated from structure)); ITRI-305 (D0N5TB, DIB003599); BLU-667 ((1S,4R)-N-((S)-1-(6-(4fluoro-1 H-pyrazole-1 -¡l)pyrid¡n-3-¡l)ethyl)-1 -methoxy-4-(4-methyl-6-((5-methyl-1 H-pyrazol-3-l)amino)pyrmidin-2-l)cyclohexane -1 carboxamide); BLU6864; DS-5010; GSK3179106; GSK3352589; NMS-E668; TAS0286 / HM05; TPX0046; and N-(3-(2(dimethylamino)ethoxy)-5-(trifluoromethyl)phenyl)-2-(4-(4-ethoxy¡-6-oxo-1,6-dih¡drop¡rid ¡n-3-¡l)-2-fluorophen¡l)acetam¡de. 152 Non-limiting examples of therapeutic agents targeting receptor tyrosine kinase (e.g., Trk) include afatinib, cabozantinib, cetuximab, crizotinib, dabrafenib, entrectinib, erlotinib, gefitinib, imatinib, lapatinib, lestaurtinib, ilotinib, pazopanib, panitumumab, pertuzumab, suniti n ib, trastuzumab, l-((3S,4R)-4-(3-fluorophenyl)-l-(2-methoxyethyl)pyrrolidin3-¡l)-3-(4-methyl-3-( 2-met¡lp¡r¡m¡din-5-¡l)-l-phenyl-IH-pyrazol-5-¡l)urea, AG 879, AR-772, AR-786, AR- 256, AR-618, AZ-23, AZ623, DS-6051, Gó 6976, GNF-5837, GTx-186, GW 441756, LOXO-101, MGCD516, PLX7486, RXDX101, VM-902A, TPX-0005, TSR- 011, GNF-4256, N-[3-[[2,3-dihydro-2-oxo-3-(1 H-pyrrole-2-ylmethylene)-1 H-indol-6-yl]amino]- 4-methylphenyl]-N'-[2fluoro-5-(trifluoromethyl)pheníl]-urea, AZ623, AZ64, (S)-5-chloro-N2-(1 -(5-fluoropíridin-2-í l)ethyl)-N4-(5-¡sopropoxy-1 H-pyrazole-3¡l)pyrimidín-2,4-dyamine, AZD7451, CEP-751, CT327, sunitinib, GNF-8625 and (R)-1 -(6-(6-(2-(3-fluorophenyl)pyrrolídin-1 ¡l)imidazo[1 ^-bjpindazin-S-ilj-p^'-bipyridinj ^'-iljpiperidin^-ol. In some embodiments, the additional therapeutic agent is a BRAF inhibitor. Non-limiting examples of a BRAF inhibitor include dabrafenib, vemurafenib (also referred to as RG7204 or PLX4032), sorafenib tosylate, PLX-4720, GDC-0879, BMS-908662 (Bristol-Meyers Squibb), LGX818 (Novartis), PLX3603 ( HofmannLaRoche), RAF265 (Novartis), RO5185426 (Hofmann-LaRoche) and GSK2118436 (GlaxoSmithKIine). Additional examples of a BRAF inhibitor are known in the art. In some embodiments, the additional therapeutic agent is an epidermal growth factor receptor (EGFR) tyrosine kinase inhibitor. For example, EGFR inhibitors may include osimertinib (merelectinib, Tagrisso), erlotinib (Tarceva), gefitinib (Iressa), cetuximab (Erbitux), necitumumab (Portrazza), neratinib (Nerlynx), lapatinib (Tykerb), panitumumab (Vectibix) and vandetanib (Caprelsa). In some embodiments, the additional therapeutic agent is an inhibitor of the Ras-Raf-MEK-ERK pathway (e.g., binimetinib, selumetinib, encorafenib, sorafenib, trametinib and vemurafenib), an inhibitor of the PI3K-Akt-mTOR pathway -S6K (e.g., everolimus, rapamycin, perifosine, temsirolimus) and other kinase inhibitors, such as baricitinib, brigatinib, capmatinib, danusertib, ibrutinib, milciclib, quercetin, regorafenib, ruxolitinib, semaxanib, AP32788, BLU285, BLU554, INCB39110, INCB40093, INCB50465, INCB52793, INCB54828, MGCD265, NMS-088, NMS-1286937, PF 477736 ((R)amino-N-[5,6-dihydro-2-(1-methyl-1 H-pyrazol-4-yl )-6-oxo-1 Hpyrrolo[4,3,2-ef][2,3]benzodiazepin-8-yl]-cyclohexanacetamide), PLX3397, PLX7486, PLX8394, PLX9486, PRN1008, PRN1371, RXDX103, RXDX106, RXDX108yTG101209 ( N-tert-butyl3-(5-methyl-2-(4-(4-methylpiperazin-1-yl)phenylamino)pyrimidin-4-ylamino)benzenesulfonamide). In some embodiments, the additional therapeutic agent is a BTK inhibitor. Non-limiting examples of BTK inhibitors include ibrutinib, acalabrutinib and zanubrutinib. In some embodiments, the additional therapeutic agent is a Bcl-2 inhibitor. Non-limiting examples of Bcl-2 inhibitors include venetoclax, navitoclax, oblimersen, obatoclax and AT-101. In some embodiments, the additional therapeutic agent is a PI3K inhibitor. Non-limiting examples of PI3K inhibitors include idelalisib, copanlisib, duvelisib, alpelisib, taselisib, buparlisib, thresholdisib and copanlisib. In some embodiments, the additional therapeutic agent is an mTOR inhibitor. Non-limiting examples of mTOR inhibitors include everolimus, temsirolimus and ridaforolimus. In some embodiments, the additional therapeutic agent is an HDAC inhibitor. Non-limiting examples QRQQcn / zznz / q / υιλι 153 HDAC inhibitors include vorinostat, romidepsin, belinostat, quidamide, panobinostat, CXD101 and abexinostat. In some embodiments, the additional therapeutic agent is a checkpoint inhibitor. Non-limiting examples of checkpoint inhibitors include ipilimumab, tremelimumab, nivolumab, pidilizumab, MPDL3208A, MEDI4736, MSB0010718C, BMS-936559, BMS-956559, BMS-935559 (MDX-1105), AMP-224, and pembrolizumab. In some embodiments, the additional therapeutic agent is a cytotoxic chemotherapeutic agent. Non-limiting examples of cytotoxic chemotherapeutic agents include arsenic trioxide, bleomycin, bendamustine, cabazitaxel, capecitabine, carboplatin, cisplatin, cyclophosphamide, cytarabine, dacarbazine, daunorubicin, docetaxel, doxorubicin, etoposide, fluorouracil, gemcitabine, irinotecan, lomustine, methotrexate, mitomycin C, oxaliplatin, paclitaxel, pemetrexed, temozolomide and vincristine. In some embodiments, the additional therapeutic agent is a treatment targeting angiogenesis. Non-limiting examples of treatments targeting angiogenesis include lenaldomide, enzastaurin, aflibercept, and bevacizumab. In some embodiments, an additional treatment or therapeutic agent may include a histidyl RNA synthetase (HRS) polypeptide or an expressed nucleotide encoding the HRS polypeptide. The term immunotherapy refers to an agent that modulates the immune system. In some embodiments, an immunotherapy may increase the expression and / or activity of an immune system regulator. In some embodiments, an immunotherapy may decrease the expression and / or activity of an immune system regulator. In some embodiments, an immunotherapy can recruit and / or enhance the activity of an immune cell. In some embodiments, the immunotherapy is a cellular immunotherapy (e.g., adoptive T cell treatment, dendritic cell treatment, natural killer cell treatment). In some embodiments, the cellular immunotherapy is sipuleucel-T (APC8015; Provenge™; Plosker (2011) Drugs 71 (1): 101-108). In some embodiments, cellular immunotherapy includes cells that express a chimeric antigen receptor (CAR). In some embodiments, cellular immunotherapy is a CAR T cell treatment. In some embodiments, the CAR T cell treatment is tisagenlecleucel (Kymria). In some embodiments, the CAR T cell treatment is axicabtagene ciloleucel (Yescarta). In some embodiments, the CAR T cell treatment is brexucabtagén autoleucel (Tecartus). In some embodiments, the CAR T cell treatment is relmacabtagene autoleucel. In some embodiments, the CAR T cell treatment is ALLO-501. In some embodiments, immunotherapy is an antibody treatment (e.g., a monoclonal antibody, a conjugated antibody, or a bispecific antibody). In some embodiments, the antibody treatment is bevacizumab (Mvasti™, Avastin®), trastuzumab (Herceptin®), avelumab (Bavencio®), rituximab (MabThera™, Rituxan®), rituximab with human hyaluronidase (Rituxan Hycela™) , edrecolomab (Panorex), daratumuab (Darzalex®), olaratumab (Lartruvo™), ofatumumab (Arzerra®), alemtuzumab (Campath®), cetuximab (Erbitux®), oregovomab, pembrolizumab (Keytruda®), dinutiximab (Unituxin®), obinutuzumab (Gazyva®), tremelimumab (CP675.206), ramucirumab (Cyramza®), ublituximab (TG-1101), panitumumab (Vectibix®), elotuzumab (Empliciti™), avelumab (Bavencio®), necitumumab (Portrazza™), cirmtuzumab (UC-961), ibritumomab (Zevalin®), isatuximab 154 (SAR650984), nimotuzumab, fresolimumab (GC1008), lirilumab (INN), mogamulizumab (Poteligeo®), ficlatuzumab (AV299), denosumab (Xgeva®), lenzilumab, avelumab, espartalizumab, pembrolizumab, utomilumab, ublituximab, blinatumomab ganitumab, urelumab , pidilizumab, amatuximab, mosunetuzumab (BTCT4465A), CD20-TCB, RO7082859, In some embodiments, the immunotherapy is an antibody-drug conjugate. In some embodiments, the antibody-drug conjugate is gemtuzumab ozogamicin (Mylotarg™), inotuzumab ozogamicin (Besponsa®), brentuximab vedotin (Adcetris®), ado-trastuzumab emtansine (TDM-1; Kadcyla®), mirvetuximab soravtansine (IMGN853 ),anetumab ravtansine, polatuzumab vedotin, loncastuximab tesirine (ADCT-402), camidanlumab tesirine (ADCT-301) or naratuximab emtansine (Debió 1562). In some embodiments, immunotherapy includes blinatumomab (AMG103; Blincyto®) or midostaurin (Rydapt). In some embodiments, the immunotherapy includes a toxin. In some embodiments, the immunotherapy is denileukin diftitox (Ontak®). In some embodiments, immunotherapy is a cytokine treatment. In some embodiments, the cytokine treatment is a treatment with interleukin 2 (IL-2), a treatment with interferon alpha (IFNa), a treatment with granulocyte colony stimulating factor (G-CSF), a treatment with interleukin 12 (IL-12), a treatment with interleukin 15 (IL-15), a treatment with interleukin 7 (IL-7), or a treatment with erythropoietin-alpha (EPO). In some embodiments, the IL-2 treatment is aldesleukin (Proleukin®). In some embodiments, the IFNa treatment is IntronA® (Roferon-A®). In some embodiments, the GCSF treatment is filgrastim (Neupogen®). In some embodiments, immunotherapy is an immune checkpoint inhibitor. In some embodiments, immunotherapy includes one or more immune checkpoint inhibitors. In some embodiments, the immune checkpoint inhibitor is a CTLA-4 inhibitor, a PD-1 inhibitor, or a PD-L1 inhibitor. In some embodiments, the CTLA-4 inhibitor is ipilimumab (Yervoy®) or tremelimumab (CP-675,206). In some embodiments, the PD-1 inhibitor is pembrolizumab (Keytruda®) or nivolumab (Opdivo®). In some embodiments, the PD-L1 inhibitor is atezolizumab (Tecentriq®), avelumab (Bavencio®), or durvalumab (Imfinzi™). In some embodiments, the immunotherapy is mRNA-based immunotherapy. In some embodiments, the mRNA-based immunotherapy is CV9104 (see, for example, Rausch et al. (2014) Human Vaccine Immunother 10(11): 3146-52; and Kubler etal. (2015) J. Immunother Cancer3 :26). In some embodiments, immunotherapy is bacillus Calmette-Guerin (BCG) treatment. In some embodiments, immunotherapy is an oncolytic virus treatment. In some embodiments, the oncolytic virus treatment is talimogene alherparepvec (T-VEC; Imlygic®). In some embodiments, immunotherapy is a cancer vaccine. In some embodiments, the cancer vaccine is a human papillomavirus (HPV) vaccine. In some embodiments, the HPV vaccine is Gardasil®, Gardasil9® or Cervarix®. In some embodiments, the cancer vaccine 155 is a vaccine against hepatitis B virus (HBV). In some embodiments, the HBV vaccine is Engerix-B®, Recombivax HB® or G1-13020 (Tarmogen®). In some embodiments, the cancer vaccine is Twinrix® or Pediarix®. In some embodiments, the cancer vaccine is BiovaxID®, Oncophage®, GVAX, ADXS11-001, ALVAC-CEA, PROSTVAC®, Rindopepimut®, CimaVax-EGF, lapuleucel-T (APC8024; Neuvenge™), GRNVAC1, GRNVAC2, GRN- 1201, hepcortespenlisimut-L (Hepko-V5), DCVAX®, SCIB1, BMT CTN 1401, PrCa VBIR, PANVAC, ProstAtak®, DPX-Survivac or viagenpumatucel-L (HS-110). In some embodiments, the immunotherapy is a peptide vaccine. In some embodiments, the peptide vaccine is nelipepimut-S (E75) (NeuVax™), IMA901 or SurVaxM (SVN53-67). In some embodiments, the cancer vaccine is an immunogenic personal neoantigen vaccine (see, for example, Ott et al. (2017) Nature 547: 217-221; Sahin et al. (2017) Nature 547: 222- 226). In some embodiments, the cancer vaccine is RGSH4K or NEO-PV-01. In some embodiments, the cancer vaccine is a DNA-based vaccine. In some embodiments, the DNA-based vaccine is a mammaglobin A DNA vaccine (see, for example, Kim etal. (2016) Oncolmmunology 5 (2): e1069940). In some embodiments, the immune system targeting agents are selected from aldesleukin, interferon alfa-2b, ipilimumab, lambrolizumab, nivolumab, prednisone and sipuleucel-T. In some embodiments, the additional treatment is radiation therapy. Non-limiting examples of radiation therapy include radioiodine treatment, external beam radiation, and radium-223 treatment. In some embodiments, the additional therapeutic agent is GSK-3368715, PF-06821497, ceralasertib; AZD6738, BI-894999, MAK-683, AZD-6738, taminadenant, TAK-981, MIK-665 or danvatirsen. QAFQCn / ZZnZ / q / ΥΙΛΙ Additional kinase inhibitors include those described, for example, in US Patent Nos. 7,514,446; 7,863,289; 8,026,247; 8,501,756; 8,552,002; 8,815,901; 8,912,204; 9,260,437; 9,273,051; US Publication No. US 2015 / 0018336; international publications No. WO 2007 / 002325; WO 2007 / 002433; WO 2008 / 080001;WO 2008 / 079906; WO 2008 / 079903; WO 2008 / 079909; WO 2008 / 080015; WO 2009 / 007748; WO 2009 / 012283;WO 2009 / 143018; WO 2009 / 143024; WO 2009 / 014637; 2009 / 152083; WO 2010 / 111527; WO 2012 / 109075;WO 2014 / 194127; WO 2015 / 112806; WO 2007 / 110344; WO 2009 / 071480; WO 2009 / 118411; WO 2010 / 031816;WO 2010 / 145998; WO 2011 / 092120; WO 2012 / 101032; WO 2012 / 139930; WO 2012 / 143248; WO 2012 / 152763;WO 2013 / 014039; WO 2013 / 102059; WO 2013 / 050448; WO 2013 / 050446; WO 2014 / 019908; WO 2014 / 072220;WO 2014 / 184069; WO 2016 / 075224; WO 2016 / 081450; WO 2016 / 022569; WO 2016 / 011141; WO 2016 / 011144;WO 2016 / 011147; WO 2015 / 191667; WO 2012 / 101029; WO 2012 / 113774; WO 2015 / 191666; WO 2015 / 161277;WO 2015 / 161274; WO 2015 / 108992; WO 2015 / 061572; WO 2015 / 058129; WO 2015 / 057873; WO 2015 / 017528; WO / 2015 / 017533; WO 2014 / 160521; and WO 2014 / 011900, each of which is incorporated herein by reference in its entirety. In some embodiments, the subject was previously administered one or more standard of care treatments for a lymphoma. In some embodiments, the preadministered standard of care is polatuzumab vedotin, selinexor, axicabtagene ciloleucel (Yescarta), tisagenlecleucel (Kymriah), bendamustine in combination with 156 rituximab and polatuzumab vedotin, tafasitamab in combination with lenalidomide or rituximab in combination with human hyaluronidase (Rituxan Hycela). In some embodiments, the subject concomitantly receives standard of care treatment for a lymphoma. In some embodiments, the standard of care is polatuzumab vedotin, selinexor, axicabtagene ciloleucel (Yescarta), tisagenlecleucel (Kymriah), bendamustine in combination with rituximab and polatuzumab vedotin, tafasitamab in combination with lenalidomide, or rituximab in combination with human hyaluronidase (Rituxan). Hycela). Although the genetic basis of tumorigenesis may vary between different types of cancer, the cellular and molecular mechanisms required for metastasis appear to be similar for all types of solid tumors. During a metastatic cascade, cancer cells lose growth inhibitory responses, undergo alterations in adhesiveness, and produce enzymes that can degrade extracellular matrix components. This leads to detachment of tumor cells from the original tumor, infiltration into the circulation through the newly formed vasculature, migration, and extravasation of tumor cells to favorable distant sites where they can form colonies. Accordingly, also provided herein are methods of inhibiting, preventing, assisting in the prevention or decreasing the symptoms of metastasis of a type of cancer in a subject in need thereof, wherein the method comprises administering to the subject an effective amount of a compound of Formula (I), or a pharmaceutically acceptable salt thereof or a pharmaceutical composition thereof. Such methods may be used in the treatment of one or more of the types of cancer described herein. See, for example, US Publication No. 2013 / 0029925; International Publication No. WO 2014 / 083567; and US Patent No. 8,568,998. See also, for example, Hezam K etal., Rev Neuroso!, January 26, 2018; 29: 93-98; Gao L, etal., Pancreas, January 2015; 44:134-143; Ding Ketal.,J Biol Chem, June 6, 2014; 289:16057-71; and Amit M etal., Oncogene, June 8, 2017; 36:3232-3239. In some embodiments, the cancer is a MALT1-associated cancer. In some embodiments, the compound of Formula (I), or a pharmaceutically acceptable salt thereof, is used in combination with an additional treatment or other therapeutic agent, as described herein. For example, a first or second MALT1 protease inhibitor. The term metastasis is a term known in the art and means the formation of an additional tumor (e.g., a solid tumor) at a site distant from a primary tumor in a subject, where the additional tumor includes cancer cells the same or similar to those of the primary tumor. Also provided are methods of decreasing the risk of developing metastasis or additional metastasis in a subject having a MALT1 associated cancer type including: selecting, identifying or diagnosing that a subject has a MALT 1 associated cancer type and administering an amount effective of a compound of Formula (I), or a pharmaceutically acceptable salt thereof, to the subject selected, identified or diagnosed with a type of cancer associated with MALT1. Also provided are methods of decreasing the risk of developing metastasis or additional metastasis in a subject having a type of cancer associated with MALT1 that includes administering an effective amount of a compound of Formula (I), or a salt acceptable from the point of pharmaceutical view of this, to a subject who has a QRQQcn / zznz / q / υιλι 157 type of cancer associated with MALT1. The decreased risk of developing metastasis or additional metastasis in a subject who has a MALT1-associated cancer type can be compared to the risk of developing metastasis or additional metastasis in the subject before treatment, or in comparison to a subject or a population from subjects who have the same type of MALT1-associated cancer or a similar type of cancer that has not received treatment or has received a different treatment. The term "risk of developing metastasis" means the risk that a subject who has a primary tumor will develop an additional tumor (e.g., a solid tumor) at a site distant from a primary tumor in a subject during a given period, where the additional tumor includes cancer cells the same or similar to those of the primary tumor. Methods for reducing the risk of developing metastasis in a subject having a type of cancer are described herein. The term risk of developing additional metastases means the risk that a subject who has a primary tumor and one or more additional tumors at sites distant from the primary tumor (where the one or more additional tumors include cancer cells the same or similar to those of the tumor primary) develop one or more additional tumors distant from the primary tumor, where the additional tumors include cancer cells the same or similar to those in the primary tumor. Methods to reduce the risk of developing additional metastasis are described herein. Some embodiments described herein provide methods for treating an autoimmune disorder (e.g., a MALT1-associated autoimmune disorder), such as rheumatoid arthritis, multiple sclerosis, and SLE, wherein the method comprises administering an effective amount of a compound of Formula (I), or a pharmaceutically acceptable salt thereof, to a subject in need. Some embodiments described herein provide methods for treating an inflammatory disorder (e.g., a MALT1-associated autoimmune disorder), such as a chronic graft-versus-host disease, wherein the method comprises administering an effective amount of a compound of Formula (I), or a pharmaceutically acceptable salt thereof, to a subject in need. Also provided is a method of inhibiting MALT1 protease activity in a mammalian cell, comprising contacting the mammalian cell with a compound of Formula (I). In some embodiments, the contacting is in vitro. In some embodiments, contacting is in vivo. In some embodiments, the contacting is in vivo, where the method comprises administering an effective amount of a compound of Formula (I), or a pharmaceutically acceptable salt thereof, to a subject has a mammalian cell that has MALT1 protease activity. In some embodiments, the mammalian cell is a mammalian immune cell. In some embodiments, the mammalian cell is a mammalian cancer cell. In some embodiments, the mammalian cancer cell is any type of cancer described herein. In some embodiments, the mammalian cancer cell is a MALT 1-associated mammalian cancer cell. Also provided is a method of inhibiting MALT1 protease activity in a mammalian cell, comprising contacting the mammalian cell with a compound of Formula (I). In some embodiments, 158 the contact is in vitro. In some embodiments, contacting is in vivo. In some embodiments, the contacting is in vivo, where the method comprises administering an effective amount of a compound of Formula (I), or a pharmaceutically acceptable salt thereof, to a mammal that has a mammalian cell that has MALT1 protease activity. In some embodiments, the mammalian cell is a mammalian immune cell. In some embodiments, the mammalian cell is a mammalian cancer cell. In some embodiments, the mammalian cancer cell is any type of cancer described herein. In some embodiments, the mammalian cancer cell is a MALT1-associated mammalian cancer cell. In some embodiments, the mammalian cell is a gastrointestinal mammalian cell. As used herein, the terms contacting or contacting refer to bringing together the indicated portions in an in vitro system or in an in vivo system. For example, contacting a MALT1 protease with a compound provided herein includes administering a compound provided herein to a subject, such as a human, having a MALT1 protease, as well as, for example, introducing of a compound provided herein in a sample containing a purified or mammalian cellular preparation containing the MALT 1 protease. Also provided herein is a method for inhibiting the proliferation of mammalian cells, in vitro or in vivo, wherein the method comprises contacting a mammalian cell with an effective amount of a compound of Formula (I), or a pharmaceutically acceptable salt thereof, or a pharmaceutical composition thereof as defined herein. A MALT1 protease inhibitor, as defined herein, includes any compound that exhibits MALT1 inhibitory activity. In some embodiments, a MALT1 protease inhibitor is selective for a MALT1 protease. Exemplary MALT1 protease inhibitors may exhibit an inhibition activity (IC50) against a MALT1 protease of less than about 1000 nM, less than about 500 nM, less than about 200 nM, less than about 100 nM, less than about 50 nM, less than about 25 nM, less than about 10 nM or less than about 1 nM, as measured in an assay described herein. In some embodiments, a MALT1 protease inhibitor may exhibit an inhibition activity (IC 50) against a MALT1 protease of less than about 25 nM, less than about 10 nM, less than about 5 nM or less than about 1 nM, as measured in an assay provided herein. As used herein, a first MALT1 protease inhibitor or first MALTΤ' inhibitor is a MALT 1 protease inhibitor as defined herein, but which does not include a compound of Formula (I), or a pharmaceutically acceptable salt thereof, as defined herein. As used herein, a second MALTT protease inhibitor or a second MALTT inhibitor is a MALT1 protease inhibitor as defined herein, but which does not include a compound of Formula (I), or a salt pharmaceutically acceptable thereof, as defined herein. When both a first and a second MALT 1 inhibitor are present in a method provided herein, the first and second MALT1 protease inhibitors are different. QRFQCn / ZZnZ / q / ΥΙΛΙ 159 An exemplary first and second MALT1 protease inhibitor are described herein. In some embodiments, a first second MALT1 protease inhibitor may be, for example, JNJ-67856633 or CTX-177. The term "effective amount" means an amount of compound that, when administered to a subject in need of such treatment, is sufficient to (i) treat a MALT1-associated disease or disorder (such as a MALT1-associated cancer), i) mitigate, improve or eliminate one or more symptoms of the particular disease, condition or disorder, or (i¡) delay the onset of one or more symptoms of the particular disease, condition or disorder described herein. The amount of a compound of Formula (I), or a pharmaceutically acceptable salt thereof, which will correspond to such amount will vary depending on factors such as the particular compound, the condition of the disease and its severity, the identity (e.g., weight) of the subject needing treatment, but may nevertheless be routinely determined by a mid-level professional. When used as pharmaceuticals, the compounds of Formula (I), including pharmaceutically acceptable salts thereof, may be administered in the form of pharmaceutical compositions. These compositions can be prepared in a manner well known in the pharmaceutical art and can be administered by a variety of routes, depending on whether local or systemic treatment is desired and depending on the area to be treated. Administration may be topical (including transdermal, epidermal, ophthalmic and mucous membrane administration, including intranasal, vaginal and rectal administration), pulmonary (for example, by inhalation or insufflation of powders or aerosols, including by nebulizer; intratracheal or intranasal) , oral or parenteral. Oral administration may include a dosage form formulated for once- or twice-daily (BID) administration. Parenteral administration includes intravenous, intra-arterial, subcutaneous, intraperitoneal, intramuscular administration or injection or infusion; or intracranial administration, for example, intrathecal or intraventricular. Parenteral administration may be in the form of a single bolus dose or may be, for example, by means of a continuous infusion pump. Pharmaceutical compositions and formulations for topical administration may include transdermal patches, ointments, lotions, creams, gels, drops, suppositories, aerosols, liquids and powders. Conventional pharmaceutical carriers, aqueous, powder or oil bases, thickeners and the like may be necessary or desirable. Also provided herein are pharmaceutical compositions containing, as the active ingredient, a compound of Formula (I) or a pharmaceutically acceptable salt thereof, in combination with one or more pharmaceutically acceptable excipients. pharmacist. For example, a pharmaceutical composition prepared by using a compound of Formula (I) or a pharmaceutically acceptable salt thereof. In some embodiments, the composition is suitable for topical administration. In making the compositions provided herein, the active ingredient is generally mixed with an excipient, diluted with an excipient, or enveloped with such a carrier in the form of, for example, a capsule, sachet, paper or other container. When the excipient functions as a diluent, it can be a solid, semi-solid or liquid material, which acts as a vehicle, carrier or medium for the active ingredient. Therefore, the compositions may be in the form of tablets, pills, powders, candies, sachets, wafers, elixirs, suspensions, emulsions, solutions, syrups, aerosols (as a solid or in a liquid medium), ointments containing, for example, example, up to 10% by weight of the active compound, gelatin capsules 160 hard and soft, suppositories, sterile injectable solutions and sterile packaged powders. In some embodiments, the composition is formulated to be administered orally. In some embodiments, the composition is a solid oral formulation. In some embodiments, the composition is formulated as a tablet or capsule. Also provided herein are pharmaceutical compositions containing a compound of Formula (I), or a pharmaceutically acceptable salt thereof, with a pharmaceutically acceptable carrier. Pharmaceutical compositions containing a compound of Formula (I) or a pharmaceutically acceptable salt thereof as the active ingredient can be prepared by intimately mixing the compound of Formula (I), or a pharmaceutically acceptable salt thereof. from a pharmaceutical point of view, with a pharmaceutical carrier in accordance with conventional techniques for the formation of pharmaceutical compounds. The carrier can take a wide variety of forms depending on the desired route of administration (e.g., oral, parenteral). In some embodiments, the composition is a solid oral composition. Suitable pharmaceutically acceptable carriers are known in the art. Descriptions of some of these pharmaceutically acceptable carriers can be found in The Handbook of Pharmaceutical Excipient, published by the American Pharmaceutical Association and the Pharmaceutical Society of Great Britain. Methods of formulating pharmaceutical compositions have been described in numerous publications, such as Pharmaceutical Dosage Forms: Tablets, Second Edition, Revised and Expanded, volumes 1-3, edited by Lieberman et al.; Pharmaceutical Dosage Forms: Parenteral Medications, Volumes 1-2, edited by Avis et al.; and Pharmaceutical Dosage Forms: Disperse Systems, volumes 1-2, edited by Lieberman et al.; published by Marcel Dekker, Inc. In preparing the compositions in oral dosage form, any of the usual pharmaceutical means can be used. Therefore, for liquid oral preparations, such as suspensions, elixirs and solutions, suitable carriers and additives include water, glycols, oils, alcohols, flavoring agents, preservatives, stabilizers, coloring agents and the like; For solid oral preparations, such as powders, capsules and tablets, suitable carriers and additives include starches, sugars, diluents, granulating agents, lubricants, binders, disintegrating agents and the like. Suitable binders include, but are not limited to, starch, gelatin, natural sugars, such as glucose or beta-lactose, corn sweeteners, natural and synthetic gums, such as acacia, tragacanth or sodium oleate, sodium stearate, magnesium stearate, sodium benzoate, sodium acetate, sodium chloride and the like. Disintegrants include, but are not limited to, starch, methylcellulose, agar, bentonite, xanthan gum and the like. Solid oral preparations may also be coated with substances such as sugars or enteric coated to modulate the primary site of absorption. For parenteral administration, the carrier will normally consist of sterile water and other ingredients may be added to increase solubility or preservation. Injectable suspensions or solutions can also be prepared by using aqueous carriers together with suitable additives. The pharmaceutical compositions herein will contain, per dosage unit, for example, tablet, capsule, powder, injection, teaspoon and the like, an amount of the active ingredient necessary QRFQCn / ZZnZ / q / ΥΙΛΙ 161 to administer an effective dose as described herein. Compositions comprising a compound of Formula (I), or a pharmaceutically acceptable salt thereof may be formulated in a unit dosage form, wherein each dose contains from about 5 to about 1000 mg (1 g), most often from about 100 mg to about 500 mg, of the active ingredient. The term unit dose form refers to physically separate units suitable as unit doses for human subjects and other subjects, where each unit contains a predetermined amount of active material (i.e., a compound of Formula (I) or an acceptable salt from the pharmaceutical point of view of this) calculated to produce the desired therapeutic effect, in association with a suitable pharmaceutical excipient. In some embodiments, the compositions provided herein contain from about 5 mg to about 50 mg of the active ingredient. A person of mid-level skill will appreciate that this includes compounds or compositions containing from about 5 mg to about 10 mg, from about 10 mg to about 15 mg, from about 15 mg to about 20 mg, of about 20 mg to about 25 mg, about 25 mg to about 30 mg, about 30 mg to about 35 mg, about 35 mg to about 40 mg, about 40 mg to about from 45 mg or from about 45 mg to about 50 mg of the active ingredient. In some embodiments, the compositions provided herein contain from about 50 mg to about 500 mg of the active ingredient. A person of mid-level skill will appreciate that this includes compounds or compositions containing from about 50 mg to about 100 mg, from about 100 mg to about 150 mg, from about 150 mg to about 200 mg, of about 200 mg to about 250 mg, about 250 mg to about 300 mg, about 350 mg to about 400 mg or about 450 mg to about 500 mg of the active ingredient. In some embodiments, the compositions provided herein contain about 10 mg, about 20 mg, about 80 mg, or about 160 mg of the active ingredient. In some embodiments, the compositions provided herein contain from about 500 mg to about 1000 mg of the active ingredient. A person of mid-level skill will appreciate that this includes compounds or compositions containing from about 500 mg to about 550 mg, from about 550 mg to about 600 mg, from about 600 mg to about 650 mg, of about 650 mg to about 700 mg, about 700 mg to about 750 mg, about 750 mg to about 800 mg, about 800 mg to about 850 mg, about 850 mg to about from 900 mg, from about 900 mg to about 950 mg or from about 950 mg to about 1000 mg of the active ingredient. The daily dose of the compound of Formula (I), or a pharmaceutically acceptable salt thereof, may vary in a wide range from 1.0 to 10,000 mg per adult human per day, or more, or any range. intermediate. For oral administration, the compositions are preferably provided in the form of tablets containing 0.01, 0.05, 0.1, 0.5,1.0, 2.5, 5.0,10.0,15.0, 25.0, 50.0,100,150,160, 200, 250 and 500 milligrams of the active ingredient for the symptomatic adjustment of the dose to the subject to be treated. An effective amount of the drug is usually delivered at a dose level of about 0.1 mg / kg to about 1000 mg / kg body weight per day, or any range in between. Preferably, the range is about 0.5 to about 500 mg / kg body weight per day, or any range. 162 intermediate. More preferably, from about 1.0 to about 250 mg / kg body weight per day, or any range in between. More preferably, from about 0.1 to about 100 mg / kg body weight per day, or any range in between. In an example, the range may be from about 0.1 to about 50.0 mg / kg body weight per day, or any amount or range in between. In another example, the range may be from about 0.1 to about 15.0 mg / kg body weight per day, or any range in between. In yet another example, the range may be from about 0.5 to about 7.5 mg / kg body weight per day, or any amount or range in between. Pharmaceutical compositions containing a compound of Formula (I), or a pharmaceutically acceptable salt thereof, may be administered in a regimen of 1 to 4 times a day or in a single daily dose. The active compound can be effective over a wide range of doses and is generally administered in a pharmaceutically effective amount. Mid-level trade people can easily determine the optimal doses to administer. It will be understood, therefore, that the amount of the compound actually administered will generally be determined by a physician and will vary depending on the relevant circumstances, including the mode of administration, the actual compound administered, the concentration of the preparation, the condition to be treated and the progression of the disease condition. Additionally, factors associated with the particular subject being treated, including the subject's response, age, weight, diet, timing of administration, and severity of the subject's symptoms, will result in the need for adjust doses. In some embodiments, the compounds provided herein may be administered in an amount ranging from about 1 mg / kg to about 100 mg / kg. In some embodiments, the compound provided herein may be administered in an amount of about 1 mg / kg to about 20 mg / kg, about 5 mg / kg to about 50 mg / kg, about from 10 mg / kg to about 40 mg / kg, from about 15 mg / kg to about 45 mg / kg, from about 20 mg / kg to about 60 mg / kg or from about 40 mg / kg at around 70 mg / kg. For example, about 5 mg / kg, about 10 mg / kg, about 15 mg / kg, about 20 mg / kg, about 25 mg / kg, about 30 mg / kg, about 35 mg / kg kg, about 40 mg / kg, about 45 mg / kg, about 50 mg / kg, about 55 mg / kg, about 60 mg / kg, about 65 mg / kg, about 70 mg / kg , about 75 mg / kg, about 80 mg / kg, about 85 mg / kg, about 90 mg / kg, about 95 mg / kg or about 100 mg / kg. A person of mid-level skill will recognize that in vivo and in vitro assays using suitable, known and generally accepted cellular and / or animal models predict the ability of a test compound to treat or prevent a given disorder. A mid-level skilled person will further recognize that human clinical trials, including first-in-human dose-range and efficacy trials, in healthy subjects and / or those suffering from a given disorder, may be completed in accordance with methods well known in clinical and medical techniques. Provided herein are pharmaceutical kits useful, for example, in the treatment of MALT 1-associated diseases or disorders, such as cancer, which includ...

Claims

1. A compound of Formula (I), or a pharmaceutically acceptable salt thereof: R2 .R2A or Cr3) hm (l) wherein: each is a single or double bond; X is N or C; Y is not C; Z is N or Cr5; wherein, when one of X and Y is N, the other of X and Y is C; n is 1, 2 or 3; R1 is hydrogen, halogen, cyano, hydroxyl, C1-C3 alkoxy, C1-C3 haloalkoxy, C1-C3 haloalkyl, -NRARB or C1-C3 alkyl optionally substituted with 1-3 substituents selected independently from hydroxyl and C1-C3 alkoxy; R2 is hydrogen, amino or halogen; R2A is hydrogen, halogen or C1-C6 alkyl; each R3 is independently halogen, hydroxyl, cyano, C3-C6 cycloalkyl, -NRARB, 5-6 membered heteroaryl optionally substituted with C1-C3 alkyl; C1-C3 alkyl optionally substituted with C1-C3 alkoxy or cyano, C1-C3 alkoxy, C1-C3 haloalkoxy or C1-C3 haloalkyl; or two R3s, together with the carbon atom to which they are attached, are joined together to form an oxo group or a C3-C8 cycloalkyl; m is 0, 1, 2 or 3;R4 is phenyl, naphthyl, 5-10 membered heteroaryl, 3-10 membered heterocyclyl, or C3-C8 cycloalkyl; wherein each R4 group is optionally substituted with 1-3 substituents selected independently from R6; R5 is hydrogen, halogen, cyano, hydroxyl, C1-C3 alkoxy, C1-C3 haloalkoxy, C1-C3 haloalkyl, -NRCRD, or C1-C3 alkyl; and each R6 is selected independently from halogen; cyano; hydroxyl; -CO2H; -N=(S=O)(C1-C3 alkyl)2, -S(=O)P(C1-C3 alkyl), -NRERF; -(C=O)NRERF; C1-C3 alkoxy optionally substituted with amino, hydroxyl, or -(C=O)NRERF; C1-C3 haloalkyl; C1-C3 haloalkoxy; 5-6 membered heteroaryl optionally substituted with 1-3 independently selected Rx groups; C1-C3 alkyl optionally substituted with 1-2 independently selected substituents from hydroxyl, -NRERF, C1-C3 alkoxy and C3-C6 cycloalkyl; C3-C6 cycloalkyl optionally substituted with hydroxyl;and -(Q)q 3-8 membered heterocycle optionally substituted with independently selected 1-3 C1-C3 alkyl; p is 1 or 2; 614 Q is -OO-NH-; q is 0 or 1; each Rx is independently selected from halogen, cyano, hydroxyl, amino, C1-C3 alkoxy, C1-C3 haloalkoxy, C1-C3 haloalkyl or C1-C6 alkyl optionally substituted with independently selected 1-3 substituents from hydroxyl, C1-C3 alkoxy and -NRGRH; RA, RB, Rc, RD are independently hydrogen, C1-C3 alkyl, or RA and RB, or Rc and RD, together with the nitrogen atom to which they are attached, join together to form a 4-6 membered heterocycle; and RE, RF, RG and RH are independently hydrogen, C1-C3 alkyl or C3-C6 cycloalkyl, or RE and RF, or RG and RH, together with the nitrogen atom to which they are attached, join together to form a 4-6 membered heterocycle optionally substituted with C1-C3 alkyl or C1-C3 alkoxy.; 2. The compound according to claim 1, wherein X is C and Y is C.

3. The compound according to claim 1, wherein X is N and Y is C.

4. The compound according to claim 1, wherein X is C and Y is N.

5. The compound according to any of claims 1-4, wherein Z is N.

6. The compound according to any of claims 1-4, wherein Z is CR5.

7. The compound according to any of claims 1-6, wherein R1 is hydrogen.

8. The compound according to any of claims 1-6, wherein R1 is a halogen.

9. The compound according to any of claims 1-6 and 8, wherein R1 is chlorine.

10. The compound according to any of claims 1-6 and 8, wherein R1 is fluoro.

11. The compound according to any of claims 1-6, wherein R1 is cyano.

12. The compound according to any of claims 1-6, wherein R1 is hydroxyl.

13. The compound according to any of claims 1-6, wherein R1 is a C1-C3 alkoxy.

14. The compound according to any of claims 1-6, wherein R1 is C1-C3 haloalkoxy.

15. The compound according to any of claims 1-6, wherein R1 is a C1-C3 haloalkyl.

16. The compound according to any of claims 1-6, wherein R1 is -NRARB.

17. The compound according to any of claims 1 or 16, wherein RA and RB are independently hydrogen or C1-C3 alkyl.

18. The compound according to any of claims 1 or 16-17, wherein one of RA and RB is hydrogen and the other of RA and RB is C1-C3 alkyl.

19. The compound according to any of claims 1 or 16-17, wherein RA and RB are both hydrogen.

20. The compound according to any of claims 1 or 16-17, wherein RA and RB are both C1-C3 alkyl.

21. The compound according to any of claims 1 or 16-17, wherein RA and RB, together with the nitrogen atom to which they are attached, are joined to form a 4-6 membered heterocycle. 615 22. The compound according to any of claims 1-6, wherein R1 is C1-C3 alkyl optionally substituted with 1-3 substituents selected independently from hydroxyl and C1-C3 alkoxy.

23. The compound according to any of claims 1-6 and 22, wherein R1 is an unsubstituted C1-C3 alkyl.

24. The compound according to any of claims 1-6 and 22, wherein R1 is a C1-C3 alkyl substituted with 1-3 substituents selected independently from hydroxyl and C1-C3 alkoxy.

25. The compound according to any of claims 1-24, wherein R2 is hydrogen.

26. The compound according to any of claims 1-24, wherein R2 is a halogen.

27. The compound according to any of claims 1-24, wherein R2 is amino.

28. The compound according to any of claims 1-27, wherein R2A is hydrogen.

29. The compound according to any of claims 1-27, wherein R2A is a halogen.

30. The compound according to any of claims 1-27, wherein R2A is C1-C6 alkyl.

31. The compound according to any of claims 1-30, wherein n is 1.

32. The compound according to any of claims 1-30, wherein n is 2.

33. The compound according to any of claims 1-30, wherein n is 3.

34. The compound according to any of claims 1-33, wherein m is 1.

35. The compound according to any of claims 1-33, wherein m is 2.

36. The compound according to any of claims 1-33, wherein m is 3.

37. The compound according to any of claims 1-36, wherein each R3 is independently halogen, cyano, C3-C6 cycloalkyl, C1-C3 alkyl optionally substituted with C1-C3 alkoxy or cyano, C1-C3 haloalkyl, C1-C3 alkoxy or C1-C3 haloalkoxy.

38. The compound according to any of claims 1-37, wherein each R3 is independently C3-C6 cycloalkyl, C1-C3 alkyl optionally substituted with C1-C3 alkoxy or cyano, C1-C3 haloalkyl, C1-C3 alkoxy or C1-C3 haloalkoxy.

39. The compound according to any of claims 1-38, wherein each R3 is independently C1-C3 alkyl or unsubstituted C1-C3 haloalkyl.

40. The compound according to any of claims 1-38, wherein each R3 is independently cyclopropyl, methyl optionally substituted with methoxy, trifluoromethyl, methoxy or trifluoromethoxy.

41. The compound according to any of claims 1-38, wherein each R3 is independently cyclopropyl, methyl, methoxymethyl or trifluoromethyl.

42. The compound according to any of claims 1-33, wherein m is 1 and R3 is methyl, methoxymethyl, trifluoromethyl or cyclopropyl.

43. The compound according to any of claims 1-33, wherein m is 2 and each R3 is methyl. 616 44. The compound according to any of claims 1-33, wherein m is 2 and each R3 is trifluoromethyl.

45. The compound according to any of claims 1-33, wherein m is 2 and one R3 is methyl and the other R3 is trifluoromethyl.

46. ​​The compound according to any of claims 1-33, wherein m is 2 and one R3 is methoxymethyl and the other R3 is trifluoromethyl.

47. The compound according to any of claims 1-33, wherein m is 2 and one R3 is methyl and the other R3 is cyclopropyl.

48. The compound according to any of claims 1-33, wherein m is 2 and one R3 is methoxymethyl and the other R3 is cyclopropyl.

49. The compound according to any of claims 1-33, wherein m is 2 and one R3 is trifluoromethyl and the other R3 is cyclopropyl.

50. The compound according to any of claims 1-33, wherein m is 2 and one R3 is methyl and the other R3 is methoxy.

51. The compound according to any of claims 1-33, wherein m is 2 and one R3 is cyclopropyl and the other R3 is methoxy.

52. The compound according to any of claims 1-33, 35-41 or 43-51, wherein the R3 groups are geminal.

53. The compound according to any of claims 1-33, wherein m is 2 and the two R3s, together with the carbon atom to which they are attached, are joined together to form an oxo group.

54. The compound according to any of claims 1-33, wherein m is 2 and the two R3s are joined to form a C3-C8 cycloalkyl.

55. The compound according to any of claims 1-33, wherein m is 0.

56. The compound according to any of claims 1-55, wherein R4 is phenyl optionally substituted with 1-3 R6 selected independently.

57. The compound according to any of claims 1-55, wherein R4 is unsubstituted phenyl.

58. The compound according to any of claims 1-55, wherein R4 is phenyl substituted with 1-2 R6 selected independently.

59. The compound according to any of claims 1-55, wherein R4 is naphthyl optionally substituted with 1-3 R6 selected independently.

60. The compound according to any of claims 1-55, wherein R4 is unsubstituted naphthyl.

61. The compound according to any one of claims 1-55, wherein R4 is a naphthyl substituted with 1-3 R6 selected independently. QRQQcn / zznz / q / υιλι 617 62. The compound according to any of claims 1-55, wherein R4 is a 56-membered heteroaryl optionally substituted with 1-3 independently selected R6.

63. The compound according to any of claims 1-55, wherein R4 is an unsubstituted 56-membered heteroaryl.

64. The compound according to any of claims 1-55 and 62, wherein R4 is a 5-6 membered heteroaryl substituted with 1-3 R6 independently selected.

65. The compound according to any of claims 1-55 or 62, wherein R4 is a 6-membered heteroaryl substituted with 1-2 independently selected R6.

66. The compound according to any of claims 63-65, wherein the 5-6 membered heteroaryl is 3-pyridyl, 4-pyridyl or 4-pyridazinyl.

67. The compound according to any of claims 63-65, wherein the 5-6 membered heteroaryl is 3-pyridyl or 4-pyridyl.

68. The compound according to any of claims 1-55, wherein R4 is C3-C8 cycloalkyl optionally substituted with independently selected 1-3 R6.

69. The compound according to any of claims 1-55, wherein R4 is a 3-10 member heterocyclyl optionally substituted with 1-3 independently selected R6.

70. The compound according to any of claims 1-55 or 69, wherein R4 is a 3-10 member heterocyclyl optionally substituted with 1-2 independently selected R6.

71. The compound according to any of claims 1-56, 58-59, 61-62 or 64-69, wherein at least one of R6 is a halogen.

72. The compound according to claim 71, wherein at least one of R6 is chlorine.

73. The compound according to any of claims 1-56, 58-59, 61-62 or 64-69, wherein at least one of R6 is cyano.

74. The compound according to any of claims 1-56, 58-59, 61-62 or 64-69, wherein at least one of R6 is hydroxyl.

75. The compound according to any of claims 1-56, 58-59, 61-62 or 64-69, wherein at least one of R6 is -CO2H.

76. The compound according to any of claims 1-56, 58-59, 61-62 or 64-69, wherein at least one of R6 is -N=(S=O)(C1-C3 alkyl or -S(=O)P(C1-C3 alkyl).

77. The compound according to any of claims 1-56, 58-59, 61-62, 64-69 or 76, wherein p is 1.

78. The compound according to any of claims 1-56, 58-59, 61-62, 64-69 or 76, wherein p is 2.

79. The compound according to any of claims 1-56, 58-59, 61-62 or 64-69, wherein at least one of R6 is -NRERF. QAFQCn / ZZnZ / q / YILI 618 80. The compound according to any of claims 1-56, 58-59, 61-62 or 64-69, wherein at least one of R6 is -(C=O)NRERF.

81. The compound according to any of claims 1-56, 58-59, 61-62, 64-69 or 79-80, wherein RE and RF are independently hydrogen or C1-C3 alkyl.

82. The compound according to any of claims 1-56, 58-59, 61-62, 64-69 or 79-81, wherein one of RE and RF is hydrogen and the other of RE and RF is C1-C3 alkyl.

83. The compound according to any of claims 1-56, 58-59, 61-62, 64-69 or 79-81, wherein RE and RF are both hydrogen.

84. The compound according to any of claims 1-56, 58-59, 61-62, 64-69 or 79-81, wherein RE and RF are both C1-C3 alkyl.

85. The compound according to any of claims 1-56, 58-59, 61-62, 64-69 or 79-80, wherein RE and RF, together with the nitrogen atom to which they are attached, are joined together to form a 4-6 membered heterocycle optionally substituted with C1-C3 alkyl or C1-C3 alkoxy.

86. The compound according to any of claims 1-56, 58-59, 61-62 or 64-69, wherein at least one of R6 is C1-C3 alkoxy optionally substituted with amino, hydroxyl or -(C=O)NRERF.

87. The compound of any one of claims 1-56, 58-59, 61-62, 64-69 or 86, wherein at least one of R6 is an unsubstituted C1-C3 alkoxy.

88. The compound of any one of claims 1-56, 58-59, 61-62, 64-69 or 86, wherein at least one of R6 is C1-C3 alkoxy substituted with amino or hydroxyl.

89. The compound of any one of claims 1-56, 58-59, 61-62 or 64-69, wherein at least one of R6 is a C1-C3 haloalkyl.

90. The compound according to any of claims 1-56, 58-59, 61-62 or 64-69, wherein at least one of R6 is difluoromethyl.

91. The compound according to any of claims 1-56, 58-59, 61-62 or 64-69, wherein at least one of R6 is a C1-C3 haloalkoxy.

92. The compound according to any of claims 1-56, 58-59, 61-62 or 64-69, wherein at least one of R6 is a 5-6 member heteroaryl optionally substituted with 1-3 independently selected Rx.

93. The compound according to any of claims 1-56, 58-59, 61-62, 64-69 or 92, wherein each Rx is independently selected from cyano, hydroxyl, C1-C3 alkoxy or C1-C6 alkyl optionally substituted with 1-3 substituents independently selected from hydroxyl, C1-C3 alkoxy and -NRGRH.

94. The compound according to any of claims 1-56, 58-59, 61-62, 64-69 or 92, wherein at least one of R6 is an unsubstituted 5-6 member heteroaryl.

95. The compound according to any one of claims 1-56, 58-59, 61-62, 64-69 or 92, wherein at least one of R6 is 1,2,3-triazol-2-yl. 619 96. The compound according to any of claims 1-56, 58-59, 61-62 or 64-69, wherein at least one of R6 is C1-C3 alkyl optionally substituted with 1-2 substituents independently selected from hydroxyl, -NRERF, C1-C3 alkoxy and C3-C6 cycloalkyl.

97. The compound according to any of claims 1-56, 58-59, 61-62 or 64-69, wherein at least one of R6 is C3-C6 cycloalkyl optionally substituted with hydroxyl.

98. The compound according to any of claims 1-56, 58-59, 61-62 or 64-69, wherein at least one of R6 is a 3-8 membered -(Q)q-heterocyclyl optionally substituted with independently selected 1-3 C1-C3 alkyl.

99. The compound according to any of claims 1-56, 58-59, 61-62, 64-69 or 98, wherein q is 0.

100. The compound according to any of claims 1-56, 58-59, 61-62, 64-69 or 98, wherein q is 1.

101. The compound according to any of claims 1-56, 58-59, 61-62, 64-69, 98 or 100, wherein Q is -O-.

102. The compound according to any of claims 1-56, 58-59, 61-62, 64-69, 98 or 100, wherein Q is -NH-.

103. The compound of any one of claims 1-55, wherein R4 is 3-pyridyl or 4-pyridyl substituted with independently selected 1-3 R6. ,R6 n 104. The compound of any one of claims 1-55 or 103, wherein R4 is where the wavy line crosses the bond connecting to the -C(=O)NH- portion of Formula (I).

105. The compound of any one of claims 1-55 or 103, wherein R4 is the wavy line crossing the bond connecting to the -C(=O)NH- portion of Formula (I). R6, wherein 106. In one of claims 1-55 or 103, wherein R4 is R6, wherein the wavy line crosses the link connecting to the -C(=O)NH- portion of Formula (I).

107. The compound of any one of claims 103-106, wherein R6 is selected from the group consisting of cyano, halogen, C1-C3 haloalkyl and C1-C3 alkoxy.

108. The compound of any one of claims 103-107, wherein R6 is selected from the group consisting of cyano, chlorine, difluoromethyl, trifluoromethyl, and methoxy. 620 R6A Aτ6B Xn 109. The compound of any one of claims 1-55 or 103, wherein R4 is where the wavy line crosses the bond connecting to the -C(=O)NH- portion of Formula (I). r6a JLa 6B 110. The compound of any one of claims 1-55 or 103, wherein R4 is R, wherein the wavy line crosses the bond connecting to the -C(=O)NH- portion of Formula (I).

111. The compound of claim 109 or 110, wherein R6A is selected from the group consisting of: cyano, halogen, unsubstituted C1-C3 alkyl, C1-C3 alkoxy, and C1-C3 haloalkyl; and R6B is selected from the group consisting of: 5-6 membered heteroaryl optionally substituted with cyano, hydroxyl, -N=(S=O)(C1-C3 alkyl)2, C1-C3 alkoxy, C1-C3 alkyl optionally substituted with 1-2 substituents independently selected from hydroxyl, C1-C3 alkoxy, and -NRGRH, or amino; -(C=O)NRERF; C1-C3 alkoxy; C1-C3 haloalkyl; C1-C3 haloalkoxy; cyano; C1-C3 alkyl; y-(Q)q-3-8 membered heterocyclyl optionally substituted with independently selected 1-3 C1-C3 alkyl.

112. The compound according to any one of claims 109-111, wherein R6A is selected from the group consisting of: cyano, fluoro, chloro, methyl, ethyl, methoxy, difluoromethyl, trifluoromethyl; and R6B is selected from the group consisting of: 1,2,3-triazol-2-yl, 4-methyl-1,2,3-triazol-2-yl, 4-hydroxymethyl-1,2,3triazol-2-yl, 4-(1,2-dihydroxyethyl)-1,2,3-triazol-2-yl, 4-(1-hydroxyethyl)-1,2,3-triazol-2-yl, 4-methoxymethyl-1,2,3-triazol-2yl, 4-methyl-1,2,3-triazol-1-yl, 4-methoxymethyl-1,2,3-triazol-2-yl, 4-amino-1,2,3-triazol-2-yl, 4-dimethylaminomethyl-1,2,3triazol-2-yl, 5-cyano-1,2,3-triazol-1-yl, 1,2,3-triazol-1-yl, 3-methyl-1,2,4-triazol-1 -yl, 5-methyl-1,2,4-triazol-1 -yl, 5amino-1,2,4-triazol-1-yl, 1 -methyl-5-amino-1,2,4-triazol-3-yl, 1,2,4-triazol-4-on-2-yl, tetrazol-5-yl, 2-methyl-tetrazol5-yl, 1-methyl-tetrazol-5-yl, imidazol-1-yl, pyrazol-1-yl, 5-cyano-pyrazol-1-yl, 1-methyl-imidazol-3-yl, 1-methyl-5amino-imidazol-3-yl, 3-methylimidazole-2-on-1-yl,1-methyl-pyrazol-3-yl, 1-methyl-pyrazol-5-yl, pyrrol-1-yl, thiazol-2-yl, sothiazolidin-2-11-1,1-dioxide, pyrrolidin-2-on-1-yl, oxazol-2-yl, oxadiazol-2-yl, 2-amino-pyramidal-4-yl, 2tetrahydrofuranyl, -(C=O)4-methylpiperazin-1-yl, -(C=O)N(CH3)2, -(C=O)NHCH3, -N=(S=O)(methyl)2, methoxy, ethoxy, difluoromethoxy, methyl, cyano., 113. The compound according to any one of claims 109-112, wherein R6A is selected from the group consisting of: cyano, chlorine, and trifluoromethyl; and R6B is selected from the group consisting of: 1,2,3-triazol-2-yl, 4-methyl-1,2,3-triazol-2-yl, 4-methyl-1,2,3-triazol-1-yl, 4-amino-1,2,3-triazol-2-yl, 5-cyano-1,2,3-triazol-1-yl, 1,2,3-triazol-1-yl, 3-methyl-1,2,4-triazol-1-yl, 5-methyl1,2,4-triazol-1-yl, 5-amino-1,2,4-triazol-1-yl, 1-methyl-5-amino-1,2,4-triazol-3-yl and 1,2,4-triazol-4-on-2-yl. QRQQcn / zznz / q / υιλι 621 R6A R6C JL r6B 114. The compound of any one of claims 1-55 or 103, wherein R4 is where the wavy line crosses the bond connecting to the -C(=O)NH- portion of Formula (I). r6a ^.R6B 115. The compound of any one of claims 1-55 or 103, wherein R4 is r6C wherein the wavy line crosses the bond connecting to the -C(=O)NH- portion of Formula (I).

116. The compound of claim 114 or 115, wherein R6A is selected from the group consisting of: cyano, halogen, C1-C3 alkyl, C1-C3 alkoxy, and C1-C3 haloalkyl; R6B is selected from the group consisting of: 5-6 member heteroaryl optionally substituted with cyano, C1-C3 alkyl, or amino; -(C=O)NRERF; C1-C3 alkoxy; C1-C3 haloalkyl; C1-C3 haloalkoxy; cyano; and C1-C3 alkyl; and R6C is selected from the group consisting of: cyano, halogen, C1-C3 alkyl, C1-C3 alkoxy, and C1-C3 haloalkyl.

117. The compound according to any one of claims 114-116, wherein R6A is selected from the group consisting of: cyano, fluoro, chloro, methyl, ethyl, methoxy, trifluoromethyl; R6B is selected from the group consisting of: 1,2,3-triazol-2-yl, 4-methyl-1,2,3-triazol-2-yl, 4-methyl-1,2,3-triazol-1-yl, 4-amino-1,2,3-triazol-2-yl, 5-cyano-1,2,3-triazol-1-yl, 1,2,3-triazol-1-yl, 3-methyl-1,2,4-triazol-1-yl, 5-methyl1,2,4-triazol-1-yl, 5-amino-1,2,4-triazol-1-yl, 1-methyl-5-amino-1,2,4-triazol-3-yl, 1,2,4-triazol-4-on-2-yl, tetrazol5-yl, 2-methyl-tetrazol-5-yl, 1-methyl-tetrazol-5-yl, imidazol-1-yl, 1-methyl-imidazol-3-yl, 1-methyl-5-amino-imidazol-3-yl, 3-methylimidazole-2-on-1-yl, 1-methyl-pyrazol-3-yl, 1-methyl-pyrazol-5-yl, pyrrol-1-yl, thiazol-2-yl, isothiazolidin-2-yl1,1-dioxide, pyrrolidin-2-on-1-yl, oxazol-2-yl, oxadiazol-2-yl, 2-amino-pyrimidin-4-yl, -(C=O)4-methylpiperazin-1yl, -(C=O)N(CH3)2, -(C=O)NHCH3, methoxy, ethoxy, difluoromethoxy, methyl, cyano;and R6C is selected from the group consisting of: cyano, fluoro, chloro, methyl, ethyl, methoxy, methyl and trifluoromethyl.; 118. The compound according to any one of claims 114-117, wherein R6A is selected from the group consisting of: cyano, chlorine, and trifluoromethyl; R6B is selected from the group consisting of: 1,2,3-triazol-2-yl, 4-methyl-1,2,3-triazol-2-yl, 4-methyl-1,2,3-triazol-1-yl, 4-amino-1,2,3-triazol-2-yl, 5-cyano-1,2,3-triazol-1-yl, 1,2,3-thazol-1-yl, 3-methyl-1,2,4-thazol-1-yl, 5-methyl1,2,4-triazol-1-yl, 5-amino-1,2,4-triazol-1-yl, 1-methyl-5-amino-1,2,4-triazol-3-yl and 1,2,4-triazol-4-on-2-yl; and R6C is selected from the group consisting of: cyano, chloro, methyl and trifluoromethyl.

119. The compound according to any of claims 1-4 or 6-118, wherein R5 is hydrogen.

120. The compound according to any of claims 1-4 or 6-118, wherein R5 is a halogen. 622 121. The compound according to any of claims 1-4, 6-118 or 120, wherein the halogen is fluorine.

122. The compound according to any of claims 1-4 or 6-118, wherein R5 is cyano.

123. The compound according to any of claims 1-4 or 6-118, wherein R5 is hydroxyl.

124. The compound according to any of claims 1-4 or 6-118, wherein R5 is a C1-C3 alkoxy.

125. The compound according to any of claims 1-4 or 6-118, wherein R5 is C1-C3 haloalkoxy.

126. The compound according to any of claims 1-4 or 6-118, wherein R5 is C1-C3 haloalkyl.

127. The compound according to any of claims 1-4 or 6-118, wherein R5 is -NRCRD.

128. The compound according to any of claims 1-4, 6-118 or 127, wherein Rc and RD are independently hydrogen or C1-C3 alkyl.

129. The compound according to any of claims 1-4, 6-118 or 127-128, wherein one of Rc and RD is hydrogen and the other of Rc and RD is C1-C3 alkyl.

130. The compound according to any of claims 1-4, 6-118 or 127-128, wherein Rc and RD are both hydrogen.

131. The compound according to any of claims 1-4, 6-118 or 127-128, wherein Rc and RD are both C1-C3 alkyl.

132. The compound according to any of claims 1-4, 6-118, or 127-128, wherein Rc and RD, together with the nitrogen atom to which they are attached, are joined together to form a 4-6 membered heterocycle.

133. The compound according to any of claims 1-4 or 6-118, wherein R5 is C1-C3 alkyl.

134. The compound according to claim 1, wherein: X is N; Yes is C; Ze is N; R1 is a halogen; R2 is hydrogen; R2A is hydrogen; m is 2 and R3 is independently C1-C3 alkyl or unsubstituted C1-C3 haloalkyl; n is 1; and R4 is a 5-6 membered heteroaryl optionally substituted with 1-2 substituents independently selected from C1-C3 haloalkyl and a 5-6 membered heteroaryl optionally substituted with 1-3 independently selected Rx. 623 135. The compound according to claim 134, wherein R1 is chlorine or fluorine.

136. The compound according to any of claims 134-135, wherein R2 is hydrogen.

137. The compound according to any of claims 134-136, wherein R2A is hydrogen.

138. The compound according to any of claims 134-137, wherein each R3 is geminal.

139. The compound according to any of claims 134-138, wherein one R3 is an unsubstituted C1-C3 alkyl and the other R3 is a C1-C3 haloalkyl.

140. The compound according to any one of claims 134-139, wherein one R3 is methyl and the other R3 is trifluoromethyl.

141. The compound according to any of claims 134-140, wherein R4 is a substituted 6-membered heteroaryl.

142. The compound according to any of claims 134-141, wherein R4 is a 6-membered heteroaryl substituted with 1,2,3-triazolyl.

143. The compound according to claim 1, wherein the compound is selected from the group consisting of the compounds in Table 1, or a pharmaceutically acceptable salt thereof.

144. A pharmaceutical composition comprising a compound according to any one of claims 1-143, or a pharmaceutically acceptable salt thereof, and at least one pharmaceutically acceptable excipient.

145. A process for preparing a compound according to any one of claims 1-143, comprising: reacting a compound of Formula (lA) R2 with R4-NH2; to form the compound according to any one of claims 1-143.

146. The process according to claim 145, wherein reacting the compound of Formula (lA) with R4-NH2 comprises reacting one of the compounds of Formula (lA) and R4-NH2 with a carbonyl equivalent selected from triphosgene and bis(trichloromethyl)carbonate to form an intermediate and then reacting the other of the compounds of Formula (lA) and R4-NH2 with the intermediate.

147. The process according to claim 146, comprising reacting R4-NH2 with one carbonyl equivalent selected from triphosgene and bis(trichloromethyl)carbonate to form the intermediate and then reacting the compound of Formula (1A) with the intermediate. 624 148. The process according to any of claims 145-147, wherein the carbonyl equivalent is triphosgene.

149. The process according to any of claims 145-147, wherein the carbonyl equivalent is bis(trichloromethyl)carbonate.

150. The process of any one of claims 145-149, wherein the compound of Formula (IA) is a compound of Formula (lAN):

151. The process of claim 150, comprising reacting a compound of Formula (lAN- with a compound of Formula (lAN-ii) R2 to form the compound of Formula (lAN).

152. The process according to claim 151, wherein the reaction of the compound of Formula (IA-Ni) with the compound of Formula (lAN-ii) is carried out in the presence of an acid.

153. The process according to claim 152, wherein the acid is hydrochloric acid or acetic acid.

154. The process of any one of claims 145-149, wherein the compound of Formula (I-A) is a compound of Formula (lAM): R2 155. The process of claim 154, comprising reacting a compound of Formula (lA- M-¡) 625 to form the compound of Formula (lAM).

156. The process according to claim 155, wherein the compound of Formula (lAMi) is reacted with an iron salt, a silane, a peroxide and an acid to form the compound of Formula (lAM).

157. The process according to claim 156, wherein the iron salt is ferric (Z)-4-oxopent-2-en-2-olate.

158. The process according to any of claims 155-157, wherein the silane is phenylsilane.

159. The process according to any of claims 155-158, wherein the peroxide is 2-tert-butylperoxy-2-methylpropane.

160. The process according to any of claims 155-159, wherein the acid is 2,2,2-trifluoroacetic acid.

161. A method for treating cancer in a subject in need, comprising administering to the subject an effective amount of a compound according to any one of claims 1-143, or a pharmaceutically acceptable salt thereof, or a pharmaceutical composition according to claim 145.

162. A method for treating a type of cancer associated with the CBM complex pathway in a subject in need, comprising administering to the subject an effective amount of a compound according to any one of claims 1-143, or a pharmaceutically acceptable salt thereof, or a pharmaceutical composition according to claim 145.

163. A method for treating a type of cancer in a subject in need, comprising: (a) identifying the type of cancer as a type of cancer associated with the CBM complex pathway; and (b) administering to the subject an effective amount of a compound according to any one of claims 1-143, or a pharmaceutically acceptable salt thereof, or a pharmaceutical composition according to claim 145.

164. The method according to claim 163, wherein the step of identifying the type of cancer in the subject as a CBM complex pathway-associated cancer type includes performing an assay to detect dysregulation in a CBM complex pathway-associated gene, a CBM complex pathway-associated protease protein, or the expression, activity, or level of any of these in a sample from the subject.

165. The method according to claim 163 or 164, further comprising obtaining a sample from the subject.

166. The method according to claim 165, wherein the sample is a biopsy sample.

167. The method according to any of claims 164-166, wherein the assay is selected from the group consisting of sequencing, immunohistochemistry, enzyme-linked immunosorbent assay, and fluorescence in situ hybridization (FISH).

168. The method according to claim 167, wherein the sequencing is pyrosequencing or next-generation sequencing.

169. A method for treating a type of cancer in a subject in need, comprising: administering to a subject an effective amount of a compound according to any one of claims 1-143, or a pharmaceutically acceptable salt thereof, or a pharmaceutical composition according to claim 145, to a subject identified with a type of cancer associated with the CBM complex pathway.

170. The method according to any one of claims 162-169, wherein the cancer type associated with the CBM complex pathway is selected from the group consisting of a cancer type associated with a cell surface receptor of the CBM complex pathway, a cancer type associated with a signal transducer between a cell surface receptor and a CBM complex, a component of a cancer type associated with the CBM complex, a cancer type associated with the protease substrate MALT1, a cancer type associated with a component of the NF-κB pathway downstream of a CBM complex, a cancer type associated with a component of the JNK pathway downstream of a CBM complex, and a combination thereof.

171. The method according to claim 170, wherein the cell surface receptor-associated cancer type of the CBM complex pathway is selected from the group consisting of a CD28-associated cancer type, a BCR-associated cancer type, a HER1-associated cancer type, a HER2-associated cancer type, and combinations thereof.

172. The method according to claim 170, wherein the cancer type associated with a signal transducer between a cell surface receptor and a CBM complex is a protein kinase C beta (PKOβ) associated cancer type, a protein kinase C theta (PCK6) associated cancer type, or a combination thereof.

173. The method according to claim 170, wherein the component of a cancer type associated with the CBM complex is selected from the group consisting of a cancer type associated with MALT1, a cancer type associated with CARD11, a cancer type associated with CARD14, a cancer type associated with CARD10, a cancer type associated with CARD9, a cancer type associated with BCL10, and combinations thereof.

174. The method according to claim 170, wherein the component of a cancer type associated with the CBM complex is selected from the group consisting of a cancer type associated with MALT 1, a cancer type associated with CARD11, a cancer type associated with BCL10, and combinations thereof.

175. The method according to claim 170, wherein the cancer type associated with the protease substrate MALT1 is selected from the group consisting of a BCL10-associated cancer type, an A20-associated cancer type, a CYLD-associated cancer type, a RelB-associated cancer type, a regnase-1-associated cancer type, a rokin-1-associated cancer type, a HOIL1-associated cancer type, a NIK-associated cancer type, a LIMAIa-associated cancer type, and a combination thereof.

176. The method according to claim 170, wherein the cancer type associated with the substrate of QRQQcn / zznz / q / uili 627 protease MALT1 is selected from the group consisting of a BCL10-associated cancer type, an A20-associated cancer type, a CYLD-associated cancer type, and combinations thereof.

177. The method according to claim 170, wherein the cancer type associated with a component of the NF-κB pathway downstream of a CBM complex is selected from the group consisting of a TAK1-associated cancer type, a TRAF6-associated cancer type, a TAB1-associated cancer type, a TAB2-associated cancer type, a TAB3-associated cancer type, an MKK7-associated cancer type, an IKKa-associated cancer type, an IKKβ-associated cancer type, an IKKy-associated cancer type, an IkBa-associated cancer type, a p50-associated cancer type, a p65 (RelA)-associated cancer type, a c-Rel-associated cancer type, and combinations thereof.

178. The method of claim 170, wherein the type of cancer associated with a component of the NF-κB pathway downstream of a CBM complex is an IKKy-associated cancer type.

179. The method of claim 170, wherein the cancer type associated with a component of the JNK pathway downstream of a CBM complex is selected from the group consisting of a JNK1-associated cancer type, a JNK2-associated cancer type, a JNK3-associated cancer type, a MYD88 transcription factor-associated cancer type, an AP-1 transcription factor-associated cancer type, and combinations thereof.

180. The method of any one of claims 162-169, wherein the cancer type associated with the CBM complex pathway is a cancer type associated with MALT1.

181. The method according to claim 180, wherein the MALT1-associated cancer type comprises an IAP2-MALT1 fusion.

182. The method according to claim 180, wherein the MALT1-associated cancer type comprises an IGH-MALT1 fusion.

183. A method for treating a type of cancer associated with MALT1 in a subject, comprising administering to a subject identified or diagnosed with a type of cancer associated with MALT1 an effective amount of a compound according to any one of claims 1-143, or a pharmaceutically acceptable salt thereof, or a pharmaceutical composition according to claim 145.

184. A method for treating cancer in a subject in need, comprising: (a) determining that the type of cancer is associated with a dysregulation of a MALT1 gene, a MALT1 protease, or the expression, activity, or level of either of these; and (b) administering to the subject an effective amount of a compound according to any one of claims 1-143, or a pharmaceutically acceptable salt thereof, or a pharmaceutical composition according to claim 145.

185. The method according to claim 184, wherein the step of determining that the type of cancer in the subject is a type of cancer associated with MALT1 includes performing an assay to detect dysregulation in an MALT1 gene, an MALT1 protease protein, or the expression, activity, or level of any of these in a sample from the subject.

186. The method according to claim 184 or 185, further comprising obtaining a sample from the subject. 628 187. The method according to claim 186, wherein the sample is a biopsy sample.

188. The method according to any of claims 185-187, wherein the assay is selected from the group consisting of sequencing, immunohistochemistry, enzyme-linked immunosorbent assay, and fluorescence in situ hybridization (FISH).

189. The method according to claim 188, wherein the sequencing is pyrosequencing or next-generation sequencing.

190. A method for inhibiting metastasis in a subject having a type of cancer that requires such treatment, comprising administering to the subject an effective amount of a compound according to any one of claims 1-143, or a pharmaceutically acceptable salt thereof, or a pharmaceutical composition according to claim 145.

191. The method according to claim 190, wherein the cancer type is a cancer type associated with the CBM complex pathway.

192. The method according to claim 191, wherein the cancer type associated with the CBM complex pathway is selected from the group consisting of a cancer type associated with a cell surface receptor of the CBM complex pathway, a cancer type associated with a signal transducer between a cell surface receptor and a CBM complex, a component of a cancer type associated with the CBM complex, a cancer type associated with the protease substrate MALT 1, a cancer type associated with a component of the NF-κB pathway downstream of a CBM complex, a cancer type associated with a component of the JNK pathway downstream of a CBM complex, and a combination thereof.

193. The method according to claim 192, wherein the cell surface receptor-associated cancer type of the CBM complex pathway is selected from the group consisting of a CD28-associated cancer type, a BCR-associated cancer type, a HER1-associated cancer type, a HER2-associated cancer type, and combinations thereof.

194. The method according to claim 192, wherein the cancer type associated with a signal transducer between a cell surface receptor and a CBM complex is a protein kinase C beta (PKOβ) associated cancer type, a protein kinase C theta (PCK6) associated cancer type, or a combination thereof.

195. The method according to claim 192, wherein the component of a cancer type associated with the CBM complex is selected from the group consisting of a cancer type associated with MALT 1, a cancer type associated with CARD11, a cancer type associated with CARD14, a cancer type associated with CARD10, a cancer type associated with CARD9, a cancer type associated with BCL10, and combinations thereof.

196. The method according to claim 192, wherein the component of a cancer type associated with the CBM complex is selected from the group consisting of a cancer type associated with MALT 1, a cancer type associated with CARD11, a cancer type associated with BCL10, and combinations thereof.

197. The method according to claim 192, wherein the cancer type associated with the protease substrate MALT1 is selected from the group consisting of a BCL10-associated cancer type, an A20-associated cancer type, a CYLD-associated cancer type, a RelB-associated cancer type, a regnase-1-associated cancer type, a rokin-1-associated cancer type, a HOIL1-associated cancer type, a NIK-associated cancer type, a LIMAIo-associated cancer type, and a combination thereof.

198. The method according to claim 192, wherein the cancer type associated with the MALT1 protease substrate is selected from the group consisting of a BCL10-associated cancer type, an A20-associated cancer type, a CYLD-associated cancer type, and combinations thereof.

199. The method according to claim 192, wherein the cancer type associated with a component of the NF-κB pathway downstream of a CBM complex is selected from the group consisting of a TAK1-associated cancer type, a TRAF6-associated cancer type, a TAB1-associated cancer type, a TAB2-associated cancer type, a TAB3-associated cancer type, an MKK7-associated cancer type, an IKKa-associated cancer type, an IKKβ-associated cancer type, an IKKy-associated cancer type, an IkBa-associated cancer type, a p50-associated cancer type, a p65 (RelA)-associated cancer type, a c-Rel-associated cancer type, and combinations thereof.

200. The method of claim 192, wherein the type of cancer associated with a component of the NF-κB pathway downstream of a CBM complex is an IKKy-associated cancer type.

201. The method of claim 192, wherein the cancer type associated with a component of the JNK pathway downstream of a CBM complex is selected from the group consisting of a JNK1-associated cancer type, a JNK2-associated cancer type, a JNK3-associated cancer type, a MYD88 transcription factor-associated cancer type, an AP-1 transcription factor-associated cancer type, and combinations thereof.

202. The method of claim 191, wherein the cancer type associated with the CBM complex pathway is a MALT 1-associated cancer type.

203. The method according to claim 202, wherein the MALT1-associated cancer type comprises an IAP2-MALT1 fusion.

204. The method according to claim 202, wherein the MALT1-associated cancer type comprises an IGH-MALT1 fusion.

205. The method according to any of claims 161-204, further comprising administering an additional treatment or therapeutic agent to the subject.

206. The method according to claim 205, wherein the additional treatment or therapeutic agent is selected from radiotherapy, cytotoxic chemotherapeutic agents, protease-targeting therapeutic agents, kinase-targeting therapeutic agents, apoptosis modulators, signal transduction inhibitors, immune system-targeting treatments, and angiogenesis-targeting treatments.

207. The method according to claim 205 or 206, wherein the compound according to any of claims 1-143 or a pharmaceutically acceptable salt thereof, or a pharmaceutical composition according to claim 145, and the additional therapeutic agent are administered simultaneously as separate doses.

208. The method according to claim 205 or 206, wherein the compound according to any 630 of claims 1-143 or a pharmaceutically acceptable salt thereof, or a pharmaceutical composition according to claim 145, and the additional therapeutic agent are administered as sequentially separate doses in any order.

209. A method for treating an autoimmune disorder in a subject in need, comprising administering to the subject an effective amount of a compound according to any one of claims 1-143, or a pharmaceutically acceptable salt thereof, or a pharmaceutical composition according to claim 145.

210. A method for treating a disease or disorder associated with the CBM complex pathway in a subject in need thereof, comprising administering to the subject an effective amount of a compound according to any one of claims 1-143, or a pharmaceutically acceptable salt thereof, or a pharmaceutical composition according to claim 145.

211. A method for treating a disease or disorder in a subject in need, comprising: (a) identifying the type of cancer as a disease or disorder associated with the CBM complex pathway; and (b) administering to the subject an effective amount of a compound according to any one of claims 1-143, or a pharmaceutically acceptable salt thereof, or a pharmaceutical composition according to claim 145.

212. A method for treating a disease or disorder in a subject in need, comprising: administering to a subject an effective amount of a compound according to any one of claims 1-143, or a pharmaceutically acceptable salt thereof, or a pharmaceutical composition according to claim 145, to a subject identified as having a disease or disorder associated with the CBM complex pathway.

213. The method according to any of claims 210-212, wherein the disease or disorder associated with the CBM complex pathway is an autoimmune disease.

214. The method according to any of claims 210-212, wherein the disease or disorder associated with the CBM complex pathway is an inflammatory disease.

215. The method according to any one of claims 210-214, wherein the cancer type associated with the CBM complex pathway is selected from the group consisting of a cancer type associated with the cell surface receptor of the CBM complex pathway, a disease or disorder associated with a signal transducer between a cell surface receptor and a CBM complex, a component of a cancer type associated with the CBM complex, a cancer type associated with the protease substrate MALT1, a disease or disorder associated with a component of the NF-κB pathway downstream of a CBM complex, a disease or disorder associated with a component of the JNK pathway downstream of a CBM complex, and a combination thereof.

216. The method according to any of claims 210-214, wherein the CBM complex pathway-associated disease or disorder is a MALT1-associated disease or disorder.

217. A method for treating an MALT1-associated autoimmune disorder in a subject, comprising administering to a subject identified or diagnosed with an MALT1-associated autoimmune disorder an effective amount of a compound according to any one of claims 1-143, or a pharmaceutically acceptable salt thereof, or a pharmaceutical composition according to claim 145.

218. A method for treating an MALT1-associated autoimmune disorder in a subject, comprising administering to a subject identified or diagnosed with an MALT1-associated autoimmune disorder an effective amount of a compound according to any one of claims 1-143, or a pharmaceutically acceptable salt thereof, or a pharmaceutical composition according to claim 145.

219. A method for treating an autoimmune disorder in a subject in need, comprising: (a) determining that the autoimmune disorder is associated with a dysregulation of a MALT1 gene, a MALT1 protease, or the expression, activity, or level of either of these; and (b) administering to the subject an effective amount of a compound according to any one of claims 1-143, or a pharmaceutically acceptable salt thereof, or a pharmaceutical composition according to claim 145.

220. A method for treating an MALT1-associated autoimmune disorder in a subject, comprising administering an effective amount of a compound according to any one of claims 1-143, or a pharmaceutically acceptable salt thereof, or a pharmaceutical composition according to claim 145 to a subject who has been determined to have an MALT1-associated autoimmune disorder.

221. A method for treating an inflammatory disorder in a subject in need, comprising administering to the subject an effective amount of a compound according to any one of claims 1-143, or a pharmaceutically acceptable salt thereof, or a pharmaceutical composition according to claim 145.

222. A method for treating an MALT1-associated inflammatory disorder in a subject, comprising administering to a subject identified or diagnosed with an MALT1-associated inflammatory disorder an effective amount of a compound according to any one of claims 1-143, or a pharmaceutically acceptable salt thereof, or a pharmaceutical composition according to claim 145.

223. A method for treating an inflammatory disorder associated with MALT1 in a subject, comprising administering to a subject identified or diagnosed with an inflammatory disorder associated with MALT1 an effective amount of a compound according to any one of claims 1-143, or a pharmaceutically acceptable salt thereof, or a pharmaceutical composition according to claim 145.

224. A method for treating an inflammatory disorder in a subject in need, comprising: (a) determining that the inflammatory disorder is associated with a dysregulation of a MALT1 gene, a MALT1 protease, or the expression, activity, or level of any of these; and (b) administering to the subject an effective amount of a compound according to any of claims 1-143, or a pharmaceutically acceptable salt thereof, or a pharmaceutical composition according to claim 145.

225. A method for treating an MALT1-associated inflammatory disorder in a subject, comprising administering an effective amount of a compound according to any one of claims 1-143, or a pharmaceutically acceptable salt thereof, or a pharmaceutical composition according to claim 145 to a subject who has been determined to have an MALT1-associated inflammatory disorder.

226. The method according to any of claims 209-225, further comprising administering an additional treatment or therapeutic agent to the subject.

227. The method according to claim 226, wherein the additional treatment or therapeutic agent is an immunotherapy.

228. The method according to claim 226 or 227, wherein the compound according to any of claims 1-143 or a pharmaceutically acceptable salt thereof, or a pharmaceutical composition according to claim 145, and the additional therapeutic agent are administered simultaneously as separate doses.

229. The method according to claim 226 or 227, wherein the compound according to any of claims 1-143 or a pharmaceutically acceptable salt thereof, or a pharmaceutical composition according to claim 145, and the additional therapeutic agent are administered as sequentially separate doses in any order.

230. A method for inhibiting the proliferation of mammalian cells, comprising contacting the mammalian cell with a compound according to any of claims 1-143, or a pharmaceutically acceptable salt thereof.

231. A method for inhibiting the activity of the CBM complex pathway in a mammalian cell, comprising contacting the mammalian cell with a compound according to any of claims 1-143, or a pharmaceutically acceptable salt thereof.

232. A method for inhibiting MALT1 protease activity in a mammalian cell, comprising contacting the mammalian cell with a compound according to any of claims 1-143, or a pharmaceutically acceptable salt thereof.

233. The method according to any of claims 230-232, wherein the contact occurs in vivo.

234. The method according to any of claims 230-232, wherein the contacting takes place in vitro.

235. The method according to any of claims 230-234, wherein the mammalian cell is a mammalian immune cell.

236. The method according to any of claims 230-235, wherein the mammalian cell is a mammalian cancer cell.

237. The method according to claim 236, wherein the mammalian cancer cell is a mammalian CBM complex pathway-associated cancer cell.

238. The method according to claim 236, wherein the mammalian cancer cell is a mammalian MALT1-associated cancer cell 633.

239. The method according to any of claims 230-238, wherein the mammalian cell has dysregulation of a MALT1 gene, a MALT1 protease protein, or the expression, activity, or level of any of these.

240. The method according to claim 239, wherein the dysregulation of a MALT1 gene, a MALT1 protease protein, or the expression, activity, or level of any of these is an IAP2-MALT1 fusion, an IGH-MALT1 fusion, or a combination thereof.

241. A use of a compound according to any of claims 1-143, or a pharmaceutically acceptable salt thereof, in the preparation of a medicament for the treatment of a disease or disorder associated with the CBM complex pathway.

242. The use according to claim 241, wherein the disease or disorder associated with the CBM complex pathway is selected from the group consisting of a cancer type associated with a cell surface receptor of the CBM complex pathway, a disease or disorder associated with a signal transducer between a cell surface receptor and a CBM complex, a component of a cancer type associated with the CBM complex, a cancer type associated with the protease substrate MALT1, a disease or disorder associated with a component of the NF-kB pathway downstream of a CBM complex, a disease or disorder associated with a component of the JNK pathway downstream of a CBM complex, and a combination thereof.

243. Use according to claim 241 or claim 242, wherein the CBM complex pathway-associated disease or disorder is a CBM complex pathway-associated autoimmune disorder.

244. Use according to claim 241 or claim 242, wherein the disease or disorder associated with the CBM complex pathway is an inflammatory disorder associated with the CBM complex pathway.

245. Use according to claim 241 or claim 242, wherein the CBM complex pathway-associated disease or disorder is a type of cancer associated with the CBM complex pathway.

246. Use according to any of claims 241-245, wherein the CBM complex pathway-associated disease or disorder is a MALT1-associated disease or disorder.

247. Use according to claim 246, wherein the MALT1-associated disease or disorder comprises dysregulation of an MALT1 gene, an MALT1 protease protein, or the expression, activity, or level of any of these.

248. Use according to claim 247, wherein the dysregulation of a MALT1 gene, a MALT1 protease protein, or the expression, activity, or level of any of these is an IAP2-MALT1 fusion, an IGHMALT1 fusion, or a combination thereof.