BCL2 is a critical apoptosis regulator that suppresses programmed cell death across diverse cell types 12. It functions by controlling mitochondrial membrane permeability and inhibiting caspase activity through two mechanisms: preventing cytochrome c release from mitochondria and binding apoptosis-activating factor (APAF-1) 3. BCL2 also functions as an autophagy inhibitor by interacting with BECN1 and AMBRA1 during non-starvation conditions 456, and may attenuate inflammation by impairing NLRP1-inflammasome activation 7. Clinically, BCL2 deregulation is central to hematologic malignancies. BCL2 activation occurs through t(14;18) translocations in follicular lymphoma 8, and BCL2 overexpression defines poor-prognosis disease when concurrent with MYC deregulation in diffuse large B-cell lymphomas 9. Loss of microRNA-15/16, which normally target BCL2, further drives overexpression in chr18 lymphocytic leukemia 8. BCL2 inhibitors like venetoclax now represent standard frontline therapy for CLL, showing superior outcomes particularly in high-risk subgroups 10. BCL2 dysregulation also associates with autoimmune disease susceptibility 11 and suppresses apoptosis in solid tumors via Akt/mTOR signaling 12.