Table 2 summarizes the major epigenetic regulators in GBM, including DNMTs, TET enzymes, EZH2, HDACs, and SWI/SNF complexes, and delineates how each modulates antigen presentation, interferon signaling, and T-cell effector function. Complementing these mechanistic insights, Figure 2 provides a schematic overview of how these tumor-intrinsic epigenetic alterations, spanning DNA hypermethylation, histone modification, chromatin remodeling, and non-coding RNA regulation, collectively converge to suppress T-cell recognition and foster immune evasion in GBM.” The gene discussed is EZH2; the disease is glioblastoma.