Researchers have discovered that the lipid molecule prostacyclin plays a key role in the repair of fetal membrane rupture. Although spontaneous healing of fetal membranes is rare and occasionally observed in clinical settings, the underlying mechanisms remain poorly understood. Using a mouse model of fetal membrane rupture, investigators examined the molecular and cellular responses at the rupture site, with a focus on prostaglandin signaling. The number of amnion mesenchymal (repair) cells at the rupture site increased as well as the enzymes creating prostacyclin. When the repair signal was activated again via treatment with an IP receptor agonist, it led to partially rescued membrane repair.