The variable dependency of AML on both BCL-2 and MCL-1 and the recent approval of venetoclax and azacytidine as a combination therapy for AML (these drugs were shown to be synergistic, as azacytidine was able to downregulate MCL-1) had led the use of combination therapies with BCL-2 inhibitors and MCL-1i for the treatment of AML. This evidence concerns the gene MCL1 and acute myeloid leukemia.