While an in vivo study showed heightened expression of EZH2 and trimethylation of H3K27 in secretory endometrium and endometriotic lesions [22,23], another cell culture study showed that inhibition of PGE2 receptors EP3 and EP4 occur concurrently with decreased EZH2 expression [24], supporting a role for PRC2 in endometriosis-associated pain. Here, EZH2 is linked to endometriosis.