Substantial progress has been achieved in our understanding of the pathogenesis of MDS through the characterization of somatic gene mutations, such as gene encoding transcription factors (TP53 or ETV6), epigenetic regulators involved in methylation (DNMT3A), the hydroxymethylation of cytosine (TET2, IDH1, IDH2) or the covalent modifications of histones (EZH2, ASXL1)6, 7. This evidence concerns the gene IDH2 and myelodysplastic syndrome.