The duplications of internal segments of the FLT3 gene (FLT3-ITD), coding for a tyrosine-kinase receptor, represent a common molecular alteration in AML, characterizing 25–30% of all cases [30]; it is associated with an adverse prognosis, which can however be mitigated in cases of treatment with FLT3 inhibitors, such as midostaurine [31]. The gene discussed is FLT3; the disease is acute myeloid leukemia.