According to the current recommendations of the WHO [1] the large and heterogeneous group of cytogenetically normal AML (CN-AML) is further stratified by the presence or absence of internal tandem duplications of fms-related tyrosine kinase 3 (FLT3-ITD), mutations of nucleophosmin (NPM1) and mutations in the CCAAT/enhancer binding protein (C/EBP) alpha (CEBPA). This evidence concerns the gene NPM1 and acute myeloid leukemia.