Moreover, we propose an epigenetic mechanism of HbF re-expression in AZA responding HR-MDS patients, through the hypomethylation of site -53 of the γ-globin gene promoter, which is a binding site of MBD2-NuRD, and the simultaneous hypermethylation of the CpG326 island of ZBTB7A gene (a known HbF suppressor); a mechanism that needs further clarification. This evidence concerns the gene MBD2 and myelodysplastic syndrome.