The upregulation of the B-cell lymphoma 2 (Bcl-2) protein, a key mediator of the mitochondrial apoptotic pathway, correlates with the survival and persistence of AML blasts.[56] Venetoclax binds to Bcl-2 and inhibits it, releasing the pro-apoptotic molecule BAX and promoting mitochondrial-mediated apoptosis. The gene discussed is BCL2; the disease is acute myeloid leukemia.