The common mutations associated with CH (epigenetic factors DNMT3A, ASXL1, TET2, DNA damage repair genes such as PPM1D, TP53, signaling genes such as JAK2, and spliceosome components SF3B1, SRSF2) can act as drivers, more often in the PLWH who develop MDS than those who develop AML, where the most common alterations are adverse/intermediate karyotype or chromosome 7 abnormalities [52]. This evidence concerns the gene DNMT3A and myelodysplastic syndrome.