Placental hypoxia during the first trimester upregulates VEGF and FLT1 to promote angiogenesis (Shore et al. 1997), but persistent hypoxia due to poor spiral artery remodeling can disrupt angiogenic balance, reducing PlGF and increasing soluble FLT1 (sFLT1), which contributes to maternal endothelial dysfunction and PE (Maynard et al. 2003; 2008). The gene discussed is FLT1; the disease is endothelial dysfunction.