Chronic ischemia of the placenta, as well as its ischemia-reperfusion, which develops in PE as a result of the impaired remodeling of the spiral arteries, promotes the release of antiangiogenic factors (soluble fms-like tyrosine kinase 1 (sFlt-1) and soluble endoglin (sEng)) and a decrease in proangiogenic factors (VEGF and placental growth factor (PlGF)) by the placenta, and the entry of these factors into the mother’s bloodstream, which leads to maternal endothelial dysfunction [59]. The gene discussed is PGF; the disease is endothelial dysfunction.