Estrogen receptor beta (ERβ) contributes to the pathophysiology of endometriosis through multiple mechanisms, including the inhibition of TNFα-induced apoptosis, induction of interleukin-1 expression, and co-stimulation of Ras-related and estrogen-regulated growth inhibitor (REGE) expression in concert with prostaglandin E2 (PGE2) under the influence of estradiol [81]. Here, ESR2 is linked to endometriosis.