Anti-apoptotic BCL-2 is overexpressed in the AML stem cell population, and it has been shown that CD34+CD38−CD123+ cells were rapidly depleted in the bone marrow after this doublet therapy, indicating that adding venetoclax to azacitidine may affect the pool of LSCs contrary to azacitidine alone [18,19]. This evidence concerns the gene BCL2 and acute myeloid leukemia.