Moreover, previous studies with venetoclax have observed variations between antiapoptotic members depending on differentiation: (i) AML cells with erythroid or megakaryocytic differentiation depend on the antiapoptotic protein B-cell lymphoma (BCL)-XL, rather than BCL-2 [51], (ii) resistant monocytic AML has a distinct transcriptomic profile, loses expression of venetoclax target BCL-2, and relies on induced myeloid leukemia cell differentiation protein Mcl-1 (MCL1) to mediate oxidative phosphorylation and survival [31], (iii) and other forms rely on BCL-2 [31]. This evidence concerns the gene MCL1 and acute myeloid leukemia.