The pronounced effects elicited by azacytidine and venetoclax administration at the level of the LSC compartment through a specific targeting of the metabolic properties of leukemic cells certainly help to understand the rate, the kinetics and the durability of responses achieved by this drug regimen; however, the very pronounced effect of this drug combination cannot be ascribed only to the effect on LSC-specific metabolic properties, but is seemingly related also to the capacity of azacytidine to induce a cellular condition that makes AML cells more susceptible to BCL-2 inhibition [90]. This evidence concerns the gene BCL2 and acute myeloid leukemia.