Abnormal placentation with insufficient maternal spiral artery remodeling is considered the predominant underlying mechanism of preeclampsia.1 The ensuing placental hypoxia leads to the release of the antiangiogenic soluble Fms-like tyrosine kinase-1 (sFlt-1) from the placenta into the maternal circulation, subsequently binding the proangiogenic placental growth factor (PlGF), thus increasing the sFlt-1/PlGF ratio.1,13 This antiangiogenic state may underlie the endothelial inflammation and dysfunction that explains the clinical spectrum. Here, PGF is linked to preeclampsia.