Internal tandem duplication of FMS-like tyrosine kinase 3 (FLT3-ITD) is one of the most common genetic alterations in human acute myeloid leukemia (AML) and confers a poor prognosis for the disease. Though several FLT3 inhibitors have been approved in AML, their clinical benefits are still unsatisfactory due to primary refractory and drug resistance. Therefore, it may be crucial to develop novel therapeutics for FLT3-ITD⁺AML.