In the remaining 45% of cases of cytogenetically normal AML (CN-AML), a number of novel molecular abnormalities have been described, such as the internal tandem duplication (ITD) in the juxtamembrane domain or mutation in the second tyrosine kinase domain (TKD) of FMS-like tyrosine kinase 3 (FLT3) gene, mutations in the nucleophosmin (NPM1) gene, CCAAT/enhancer binding protein-α (CEBPA) gene and in the Wilms’ tumour gene and partial tandem duplication (PTD) of the mixed-lineage leukaemia (MLL) gene (reviewed by Mrózek et al, 2007). This evidence concerns the gene NPM1 and acute myeloid leukemia.