BCL2L2 (BCL2 like 2) is an anti-apoptotic protein that promotes cell survival through suppression of pro-apoptotic pathways. The protein contains four BCL-2 homology domains 1 and functions as a key regulator of the intrinsic apoptotic pathway, blocking mitochondrial outer membrane permeabilization and cytochrome c release 2. BCL2L2 exerts its pro-survival effects by restraining BAX activity 3 and is particularly important in regulating cell survival during development and differentiation. In cancer biology, BCL2L2 promotes tumorigenesis through multiple mechanisms. miR-29b and miR-16 suppress BCL2L2 expression to inhibit glioblastoma and oral squamous cell carcinoma progression respectively, demonstrating BCL2L2's role in cancer cell survival and stemness maintenance 45. A glioblastoma-associated Bcl2l2-Pabpn1 fusion transcript promotes tumor progression by blocking Bax activity and activating PI3K/AKT signaling 3. In megakaryocyte biology, BCL2L2 overexpression decreases apoptosis, increases proplatelet formation by 58%, and is positively associated with platelet number in healthy donors 6. BCL2L2 gene expression is regulated through alternative splicing mechanisms involving 5' UTR elements and upstream open reading frames 1, with splice isoform-specific targeting representing a potential therapeutic approach in cancer 7. Additionally, the miR-140/BCL2L2 axis regulates smooth muscle cell apoptosis in intracranial aneurysm formation 8.