Commentary tion, and PGF2α in the induction of labor. Additional roles may at present be obscured by redundancies in the system. For example, myometrial TPs, FPs, EP1s, and EP3s may all mediate uterotonic effects of their ligands (28, 29). Both FP and EP agonists are used in the induction of labor, and NSAIDs may prevent preterm labor (30). A refined understanding of the role of PGE2 in inflammation, blood pressure homeostasis, and reproduction may reveal new therapeutic opportunities for EP subtype–specific agonists and antagonists. Also, given the marked induction of COX-2 at the site of the implanting blastocyst and in decidual cells (18), elucidation of the effects of selective COX-2 inhibitors on the reproductive process in humans would seem timely.