In AML, clonal evolution results in a heterogeneous disease that, in turn, contributes to treatment resistance and poor prognosis.1, 2, 3 Internal tandem duplication (ITD) mutations in the FMS‐like tyrosine kinase 3 (FLT3) are among the most common driver mutations in AML, occurring in ∼25% of patients with newly diagnosed disease.4 Patients with FLT3‐ITD‐mutated AML have a particularly poor prognosis following conventional chemotherapy,3, 4 making FLT3 an attractive therapeutic target. This evidence concerns the gene FLT3 and acute myeloid leukemia.