This particular alteration inhibits PRC2 activity and results in a global reduction in H3K27 methylation in a mouse model of DMG tumourigenesis and in human DMG cells, with the exception of retained H3K27me3 on the tumour suppressor CDKN2A locus, potentially due to EZH2 activity.323 Thus, EZH2 has been suggested as a potential therapeutic target in DMG. This evidence concerns the gene EZH2 and neoplasm.