Given that placental pericytes dysfunction is linked to preeclampsia (8) and the fact that dydrogesterone and 17-OHPC are now being investigated as a potential therapeutic intervention for preeclampsia (19, 20), our results support the notion that Kir7.1 is a promising molecular target to potently control uteroplacental physiology. Here, KCNJ13 is linked to preeclampsia.