The ensuing highly antiangiogenic state subsequently triggers the release of the vasoconstrictor ET-1 (endothelin-1), further inducing the widespread maternal endothelial dysfunction typically associated with this syndrome.3,4 Ideally, mitigating the release of sFlt-1 and ET-1 or enhancing PlGF production should resolve the angiogenic imbalance, thereby delaying disease progression in women with preeclampsia. This evidence concerns the gene PGF and preeclampsia.