In the context of a pro-inflammatory endometrium, one recent study (352) investigated the pharmacological effects of selective inhibition of prostaglandin receptors (EP2/EP4) by using a chimeric mouse model of endometriosis and found that endometrial functional receptivity can potentially be restored the interaction among prostaglandin E2 (PGE2), estrogens and progesterone. The gene discussed is PTGER4; the disease is endometriosis.