EZH2 and prostate carcinoma: The loss of EZH2 catalytic function, by chemical inhibition, led to increased dsRNA levels, loss of H3K27me3 and concurrent gain of H3K27 acetylation (H3K27ac), a marker of transcriptional activation, at 302 genes containing endogenous retroviral sequences in in vitro and in vivo models of prostate cancer (91).