In support of the idea that targeting antiapoptotic Bcl-2 proteins with BH3 mimetics may increase NK cell-mediated cytotoxicity, a recent report has described that inhibition of Mcl-1, but not Bcl-2, increased the therapeutic efficiency of NK cells against acute myeloid leukemia (AML) cells [47]. This evidence concerns the gene BCL2 and acute myeloid leukemia.