Importantly, PRC2 inhibitors alleviated the transcriptional inhibition of MHC‐I to rebuild CD8+ T cell‐mediated antitumor immunity.[82] Moreover, BRD4 inhibitors (BRD4i, e.g., JQ1) decreased PD‐L1 expression and increased MHC‐I expression on prostate cancer cells, which led to enhanced tumor immunogenicity and intratumoral CTL infiltration; thus, finally resensitizing pancreatic cancer to immune checkpoint blockade (ICB) therapy.[83]. This evidence concerns the gene CD8A and neoplasm.