FLT3 and acute myeloid leukemia: The high frequency of NPM1 mutations in normal-karyotype AMLs and the fact that cytoplasmic NPM1 fails to carry out its normal functions such as binding to proteins and transferring them lead to the hypothesis that mutations in NPM1 would be a primary event in leukemogenesis.20 Therefore, it seems that NPM1 mutations lead to acquiring additional genetic changes in AML leukemic cells.21 Moreover, NPM1 mutations often occur in association with FLT3/ITD mutations.11 FLT3 is a receptor tyrosine kinase with important roles in hematopoietic stem/progenitor cell survival and proliferation.22