While quizartinib demonstrated single-agent activity in relapsed/refractory (R/R) FLT3-ITD–positive (FLT3-ITD +) AML patients [22], treatment-emergent FLT3-TKD mutations leading to drug resistance [15] and myelosuppression due to quizartinib’s effects on c-kit [23] are of concern. The gene discussed is FLT3; the disease is acute myeloid leukemia.