Few AML-associated genetic lesions are exclusively found in AML, and even those such as FLT3 internal tandem duplications or NPM1 mutations, which are rarely found in clinical contexts other than AML, yield prominent myeloproliferative phenotypes when modeled in mice (Kelly et al., 2002; Vassiliou et al., 2011). This evidence concerns the gene NPM1 and acute myeloid leukemia.