EZH2 and neoplasm: In both experimental systems, MHC-I and MHC-II expression were significantly reduced in mutant Ezh2 mice compared to wild-type mice, with reduced infiltration of CD3, CD4 and CD8 T cells in the tumor microenvironment, establishing Ezh2 gain-of-function mutation as a driver of MHC downregulation in GC lymphomagenesis, and eventually favoring immune escape.