More specifically, while BIM knock-down showed a trend towards abrogating single-agent venetoclax activity, the change was not significant, suggesting that, at least in the two AML cell lines analyzed, single-agent venetoclax operates largely independent of BIM through the classic displacement model [49], whereby BCL-2 directly interacts with BAX/BAK to negatively regulate MOMP. This evidence concerns the gene BAK1 and acute myeloid leukemia.