The B-cell lymphoma (BCL-2) family of proteins, including anti-apoptotic (BCL-2, BCL-XL, MCL-1) and pro-apoptotic proteins (BAX, BAK and BH3-only), are essential regulators of programmed cell death and the dysregulation of their interplay has been demonstrated to be a key mechanism of leukemic blast survival in both acute myeloid leukemia (AML) and ALL [106]. This evidence concerns the gene BAX and acute myeloid leukemia.