EZH2 and neoplasm: In SMARCB1/SNF5-deficient tumor cells, EZH2 inhibitor treatment can increase p16INK4a expression by lowering the level of tri-methylated H3K27 in the p16INK4a gene region, which demonstrates that EZH2 epigenetically silences the expression of p16INK4a by catalyzing H3K27 tri-methylation [18, 19].