FMS-like tyrosine kinase 3 (FLT3) internal tandem duplication (FLT3-ITD) mutations and FLT3 tyrosine kinase domain (FLT3-TKD) mutations promote constitutive activation of FLT3 signaling which ultimately favour the proliferation of AML cells [5]. The gene discussed is FLT3; the disease is acute myeloid leukemia.