Mutations via internal tandem duplication (ITD) or in the tyrosine kinase domain (TKD) lead to aberrant cell proliferation due to constitutively active FLT3 kinase and are present in around 25% of AML cases, with almost a third of NPM1 mutations occurring in association with a FLT3 mutation [66]. The gene discussed is NPM1; the disease is acute myeloid leukemia.