We showed that depletion of BCL2 via both gene silencing and chemical inhibition in addition to FLT3 inhibition increased cell death in FLT3-ITD cell lines and primary AML patient samples beyond that of each perturbation alone, an effect which was not observed to the same extent in the case of FLT3-WT. This evidence concerns the gene FLT3 and acute myeloid leukemia.