FLT3 and acute myeloid leukemia: AML often develops through the acquisition of multiple somatic mutations with a specific temporal order, where mutations in epigenetic modifying proteins (IDH1, IDH2, TET2, DNMT3A, and ASXL1) or other (TP53, JAK2, SRSF2, and SF3B1) proteins are acquired in the founding clone, while mutations in proteins effecting signaling (FLT3, KIT, PTPN11, N-RAS, KRAS, and CBL) and epigenetic re-programing (NPM1) are secondary mutations acquired during leukemogenesis [14].