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. The gene discussed is CDKN2B; the disease is myelodysplastic syndrome.