The observation that antiapoptotic proteins, including BCL2, BCLXL, and MCL1, are frequently overexpressed in AML and are associated with resistance to chemotherapy, eventually led to the addition of venetoclax, an oral selective small molecule inhibitor of BCL2, to LDAC or HMA therapy, initially in older adults with primary or secondary AML who were ineligible for conventional chemotherapy[26]. This evidence concerns the gene BCL2L1 and acute myeloid leukemia.