TP-0903 retained activity in AML with FLT3-ITD and TKD mutations — including the F691L gatekeeper mutation, which promotes varying degrees of resistance to current FLT3 TKIs — and was able to overcome FLT3 TKI resistance due to bone marrow microenvironment–mediated stromal cell, cytokine, chemokine, and growth factor support. The gene discussed is FLT3; the disease is acute myeloid leukemia.