“…Nevertheless, PRC2-independent functions of EZH2, e.g., the modification of protein activity by methylation or direct binding, have also been described in different cancer entities [ 25 , 26 , 27 , 28 , 29 , 30 ]. EZH2-mediated gene-silencing and other epigenetic mechanisms in cancer development and progression have gained increasing interest and offer new treatment options [ 19 , 31 , 32 ]. In most cancer entities (e.g., pancreatic cancer, breast cancer, prostate cancer, lung cancer), EZH2 is clearly associated with pro-tumorigenic and tumor-progressive characteristics [ 33 , 34 , 35 , 36 , 37 , 38 , 39 ].…”