In conclusion, the results presented here indicate that Bcl-2/Bcl-XL and Mcl-1 act in a redundant fashion as effectors of BMM-mediated AML drug resistance and indicate that for BH3-mimetic-based treatment of AML the focus must be broadened from sole targeting of Bcl-2 to the additional inhibition or repression of Mcl-1. This evidence concerns the gene BCL2L1 and acute myeloid leukemia.