DNMT3A and endometriosis: The maintenance of DNMT3A level by the inflammation pathway has been implied, since inhibition of PGE2-EP2/EP4 biosynthesis inhibits growth, invasion, migration, adhesion, and survival of endometriotic epithelial and stromal cells by upregulating proteins associated with these pathways, thus impeding growth of endometriosis (Figure 3) [112].