The two-stage hypothesis suggests that PE develops in two stages: impaired placentation due to inadequate trophoblast invasion, leading to poor spiral artery remodeling and placental hypoxia, followed by a maternal systemic response involving the release of anti-angiogenic factors (soluble fms-like tyrosine kinase-1 (sFlt-1) and soluble endoglin (sEng)), causing widespread endothelial dysfunction and systemic inflammation [18,19]. The gene discussed is FLT1; the disease is endothelial dysfunction.