The high selectivity of MLN0128, evidenced by its high potency against mTORC1/2 downstream targets S6, 4EBP1, and AKT and coupled with negligible effects on other signaling pathways, provides the impetus for testing MLN0128 in AML clinical trials, with emphasis on AML patients harboring FLT3 mutations. The gene discussed is FLT3; the disease is acute myeloid leukemia.