It was recently reported that a large proportion of M-MDSCs could differentiate into PMN-MDSCs in tumor-bearing mice, and transcriptional silencing of the retinoblastoma gene (Rb1) via epigenetic modifications by histone deacetylase 2 (HDAC-2) mediated this phenotype conversion.57 In the periphery, the existence of tumor-derived inflammatory factors promotes the differentiation of M-MDSCs into immunosuppressive macrophages as well as inhibits the functional maturation of DCs. The gene discussed is RB1; the disease is neoplasm.