Given that AKT has been identified as a downstream effector of FLT3 signaling (Fathi and Chen, 2011; Gilliland and Griffin, 2002), BM stromal factors likely confer dependence of FLT3-ITD AML cells on ATM following FLT3 inhibition to maintain AKT activity, followed by subsequent activation of mTORC1. The gene discussed is AKT1; the disease is acute myeloid leukemia.