Excessive placental antiangiogenic factor (soluble fms-like tyrosine kinase 1, sFlt1) antagonizes vascular endothelial growth factor (VEGF) and placental growth factor (PlGF), thereby inducing oxidative stress, lipid peroxidation, endothelial dysfunction, and peripheral vasoconstriction during the second phase of PE pathogenesis [100]. The gene discussed is VEGFA; the disease is endothelial dysfunction.