This is due to VEGF and PlGF binding to circulating sFlt-1 instead of the target receptor, resulting in vasoconstriction and endothelial dysfunction, including increased secretion of endothelin-1, a vasoconstrictor, and a reduction in the generation of endothelial nitric oxide, a potent vasodilator (Lam et al., 2005; Karumanchi, 2016; Rana et al., 2020). The gene discussed is EDN1; the disease is endothelial dysfunction.