Overall, these data provide a rationale that has prompted us to analyse a series of 195 de novo AML patients in order to establish at first time, the relationships between these strong mediators of gene expression (DNMT3A/B and EVI1) and other well-known biomarkers such as Nucleophosmin (NPM1), fms-like tyrosine kinase-3 (FLT3) mutations, partial tandem duplications of mixed-lineage leukemia gene (MLL/PTD) and HOXA9 expression level. This evidence concerns the gene KMT2A and acute myeloid leukemia.