This molecular profile is defined by recurrent alterations in genes associated with signaling pathways (FLT3, NRAS, KRAS), tumor suppression (WT1), chromatin organization (ARID1B and ARID1A), oncogenes (SALL4, MED12, NSD1), and rarer mutations in other AML-pathways, including NPM1 mutations, DNA methylation (DNMT3A, IDH1/2 and TET2), or epigenetic regulation (ASXL1) [115,116,123,128]. This evidence concerns the gene NRAS and acute myeloid leukemia.