As clinical resistance can arise in AML patients coharboring FLT3-ITD and FLT3 wt due to the stimulation effects of FLT3 ligand and subsequent hyper-activation of AKT signaling, A674563 as a dual AKT and FLT3-ITD inhibitor could potentially serve as a novel approach to effectively treat FLT3-ITD-positive AML. This evidence concerns the gene AKT1 and acute myeloid leukemia.