Equally relevant is the degree of activity against wild-type (WT) FLT3: although inhibition of WT FLT3 may contribute to toxicity in the setting of regenerating marrow, it also raises the possibility of therapeutic benefit in FLT3–wild-type AML, as suggested by early quizartinib data and ongoing trials in this population [49]. The gene discussed is FLT3; the disease is acute myeloid leukemia.