PRF1 and neoplasm: This phenomenon was ascribed to reduced H3K9me3 deposition at regulatory regions of various immune-related genes, including IL-21R, IFNγ, perforin, and granzyme B. The epigenetic de-repression of these genes supported the expansion of CD8+ T cells, TME conversion to ”hot”, the immunogenic phenotype, and tumor growth inhibition in HP1γ-deficient mice bearing ovarian tumors or neuroblastoma cells [146,147].