Makishima et al. in their analysis on the dynamics of clonal evolution in MDS reported the analysis of the mutational profiling of 33 secondary AMLs developed from a preceding MDS and showed that mutations in seven genes, including IDH1, IDH2, FLT3, PTPN11, WT1, NPM1, and NRAS were significantly enriched in s-AML compared to high-risk MDSs; the presence of these mutations in high-risk MDSs reduce their time of progression to AML [21]. This evidence concerns the gene PTPN11 and myelodysplastic syndrome.