For instance, in GBM patients, besides an overall surge in MDSC quantity compared to healthy controls, there’s a conspicuous shift with an increase in PMN-MDSCs and M-MDSCs and a significant decrease in e-MDSCs.71,72 Peripheral and tumor tissue MDSCs can further differentiate, exemplified by M-MDSCs differentiating into PMN-MDSCs in tumor-bearing mice through histone deacetylase 2 (HDAC-2) mediated epigenetic silencing of the retinoblastoma gene (Rb1).73 This population shift further amplifies immunosuppression. Here, HDAC2 is linked to glioblastoma.