About 15 million babies are born preterm each year, according to the World Health Organization. And current therapies don’t work well at preventing preterm birth. Evidence suggests that increases in intracellular Ca2+ levels help induce contractions, but blocking the main calcium channel doesn’t prolong gestation. David N. Cornfield of Stanford University and coworkers now show that a nonselective calcium channel, transient receptor potential vanilloid 4 (TRPV4), plays a role in controlling contractions in uterine tissue (Sci. Transl. Med. 2015, DOI: 10.1126/scitranslmed.aad0376). Expression of this protein in uterine cell membranes increases as pregnancy progresses. Uterine contractility decreases when TRPV4 is blocked and increases when it’s stimulated. In a mouse model of preterm labor, blocking TRPV4 delayed the onset of labor. The team gave pregnant mice RU-486 to chemically induce contractions. Giving the mice the TRPV4 antagonist HC 067047 delayed delivery of the pups. On the basis of these results, the researchers propose that TRPV4 may be a potential therapeutic target for preventing preterm labor.