FLT3 and acute myeloid leukemia: Treatment with a first-generation FLT3 inhibitor, sorafenib, restored the HSC compartment in these mice and ablated MPNs, demonstrating the efficacy in targeting FLT3 as a therapeutic means.141 However, it still stands that AML is a heterogeneous disease, and in fact, untreated AML is frequently a polyclonal disease, where the FLT3 mutation is found in only a subset of the bulk AML population.142 Additionally, FLT3 inhibitors have been shown to have off-target effects, and the toxicity may limit efficacy when translating to clinical care.44