Whole genome sequencing techniques have been able to establish that the progression of MDS to AML is defined by the persistence of a founder clone, and the emergence or growth of at least one subclone, carrying new mutations (mostly FLT3, NPM1, NRAS, PTPN11, WT1, IDH1 and IDH2). This evidence concerns the gene FLT3 and acute myeloid leukemia.