Genomic and functional studies have identified two classes of mutations, which cooperate during AML development. Class I mutations, which confer proliferative and survival advantage to hematopoietic stem cells, an example is the occurrence of mutations in NRAS or KRAS genes, or mutations affecting receptor tyrosine kinase FLT3.Class II mutations characterize for promoting self-renewal and blocking differentiation of hematopoietic stem cells. These mutations include certain translocation, an example of this type of mutations is gene MLL1 derived from t(8;21) (AML1-ETO).Major mutations in AML are commonly detected in cytogenetically Normal (CN) cases representing 40% to 50% of all AML.