The molecular mechanisms of progressive MDS and de novo AML require joint actions of factors involved in epigenetic modification, signal transduction, RNA splicing and cohesion pathways [10, 27], the absence of mutations in DNA repair and cell cycle regulation as well as the increase of transcription-related mutations (other than those in NPM1 and WT1), which might indicate a progressive expansion capacity of abnormal clones in de novo AML [27]. This evidence concerns the gene NPM1 and myelodysplastic syndrome.