The data indicate that DZNep-mediated suppression of EZH2 activity, as measured by a decrease in the H2K27Me2 and H3K27Me3 histone marks, resulted in inhibition of cell-cycle progression and increased apoptosis, supporting a role of EZH2 in the progression of MDS to a more advanced stage, in conceptual agreement with stage-specific epigenetic alterations in MDS, as reported by others [32]. This evidence concerns the gene EZH2 and myelodysplastic syndrome.