Internal tandem duplications of the Fms-like tyrosine kinase 3 receptor (FLT3-ITD) are found in ∼20% of AML patients and are associated with poorer outcomes.1 Recent efforts to target FLT3 with the tyrosine kinase inhibitor quizartinib have demonstrated efficacy by inducing CRs in patients with refractory disease; however, point mutations within the kinase domain of FLT3 confer quizartinib resistance and have been detected in patients.31 Therefore, treatments that modulate FLT3 expression independent of kinase inhibition are of particular interest. This evidence concerns the gene FLT3 and acute myeloid leukemia.