FLT3 mutations, either as an internal tandem duplication (FLT3-ITD) or tyrosine kinase domain point mutation (FLT3-TKD), occur in 25% and 7% of AML, respectively, and constitutively activate the FLT3 proliferation and cell survival pathway [3, 14]. The gene discussed is FLT3; the disease is acute myeloid leukemia.