We have shown that the small molecule inhibitor ABT‐199 can disrupt this interaction in AML.21 However, ABT‐199 treatment also caused increased sequestration of Bim by Mcl‐1 in ABT‐199‐resistant AML cells.21 Previous studies by our lab and others have shown that ABT‐199 treatment increases levels of Mcl‐1 in resistant AML cells lines and primary AML patient samples by enhancing Mcl‐1 protein stability rather than gene transcription.14, 22 Furthermore, CRISPR knockdown of Mcl‐1 significantly enhanced ABT‐199‐induced apoptosis in AML cells. This evidence concerns the gene BCL2L11 and acute myeloid leukemia.