Point mutations in FLT3 have also been reported in acute myeloid leukemia (AML) patients harboring FLT3 internal tandem duplications who relapsed after a transient response to quizartinib, a potent FLT3 inhibitor, suggesting that at least some AML patients may acquire these mutations early during disease evolution [68]. The gene discussed is FLT3; the disease is acute myeloid leukemia.