Over the 15 years since the discovery of the mutated receptor and its clinical significance, more than a dozen different tyrosine kinase inhibitors (TKI) have been developed and tested preclinically, and many have shown to selectively induce cell death in FLT3 mutated AML blasts by suppressing FLT3 autophosphorylation and downstream signaling pathways [40,41,42]. The gene discussed is FLT3; the disease is acute myeloid leukemia.