In consistent to those studies, disrupting EZH2 activity in Tregs could selectively deplete T cells and alter their functions in murine colorectal tumor, enhancing the recruitment of CD8+ and CD4+ T cells and remodeling the TME [118], whilst high expression of EZH2 was shown to improve the escape from immunotherapy in neuroblastoma through transcriptional downregulation of major histocompatibility complex (MHC)-1 genes by H3K27me3 modification [216]. This evidence concerns the gene EZH2 and colorectal neoplasm.