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The mechanisms of apoptosis may help elucidate the pathologies of uncontrolled cell growth or death. Apoptosis is under the mediation of 2 major pathways: the extrinsic or death receptor pathway and the intrinsic or mitochondrial pathway.[1][2] The intrinsic pathway is controlled and regulated by the Bcl-2 (B-cell lymphoma 2) family of proteins. The proteins in this family can be classified by their anti-apoptotic (Bcl-2, Bcl-x, Bcl-w, Mcl-1, and A1/Bfl-1) or pro-apoptotic (Bax, Bak, and Bok/Mtd) actions.[3] Both pathways result in caspase activation, leading to the termination of cell life.[4] The BAX gene (Bcl-2 Associated X-protein) is a pro-apoptotic member of the Bcl-2 gene family; it encodes a 21-kDa protein named BAX-alpha, whose association with Bcl-2 researchers believe plays a critical role in regulating intrinsic apoptosis.[4]

Because of the Bax gene's role in cell apoptosis, dysfunction carries links to various pathologies related to cell accumulation (i.e., cancer) or cell loss (ie, heart failure, Alzheimer disease).[2] Tumorigenesis largely depends on the cell's ability to overcome cell cycle regulators and apoptosis. Research has shown that both loss of function and gain of function mutations in Bcl-2 family proteins, including Bax, increase the likelihood of human tumorigenesis.[13] Research demonstrates that Bax deletion increases the oncogenic gene activation and the progression of certain cancers, such as Philadelphia-positive leukemia.[12]