VEN, a selective BCL-2 inhibitor, has shown efficacy in AML[13]; however, monotherapy is prone to drug resistance.[14] AZA enhances VEN’s antitumor effect by activating the transcription of the proapoptotic protein NOXA.[15] The combination of VEN and AZA induces strong and long-lasting antileukemic effects by blocking the energy metabolism of leukemic stem cells. This evidence concerns the gene PMAIP1 and acute myeloid leukemia.