The second stage of PE is thought to be the maternal response to abnormal placentation resulting from endothelial dysfunction and an imbalance in circulating angiogenic/vasculogenic factors such as soluble vascular endothelial growth factor receptor-1 (VEGFR-1, sFlt-1), placental growth factor (PlGF), and the transforming growth factor-beta receptor endoglin (CD105) (reviewed by [9, 11]). The gene discussed is FLT1; the disease is endothelial dysfunction.