Due to the presence of a hyper-methylated profile of anti-oncogene in MDS [124, 125], the common use of drugs such as AZA and decitabine, and also, due to the proven role of HO-1 in preventing the demethylation of anti-oncogenes such as p15 and p16, as well as the induction of BcL-2, DNMT1, EZH2 and cell cycle progression by HO-1, it can be said with high confidence that HO-1inhibition in MDS (at least in high-risk patients) is beneficial and increases the effectiveness of the mentioned drugs and could even reduce the required dose to alleviate side effects. This evidence concerns the gene EZH2 and myelodysplastic syndrome.