Increased levels of the antiangiogenic factors, soluble fms-like tyrosine kinase 1 (sFlt-1), and soluble Endoglin (sEng) trap circulating vascular endothelial growth factor (VEGF), placental growth factor (PlGF), and transforming growth factor β (TGFβ), respectively, decreasing their free levels, leading to endothelial dysfunction and the clinical manifestations of the disease [66]. This evidence concerns the gene TGFB1 and endothelial dysfunction.