The increase in ESR2 levels in lesions may be responsible for increased lesion survival and inflammation because E2 can act through ESR2 to induce the cyclooxygenase-II (COX-2)-prostaglandin E2 (PGE2) feedback loop [176], which is well known to increase the inflammation and pathology of endometriosis [177]. This evidence concerns the gene ESR2 and endometriosis.