Recent studies suggest, that circulating anti-angiogenic substances such as a soluble splice variant of the VEGF-receptor Flt-1 (sFlt-1) and a soluble form of the TGF-β-receptor Endoglin, soluble endoglin (sEng) act in concert to induce endothelial dysfunction and the maternal syndrome of preeclampsia [2]–[4]. This evidence concerns the gene FLT1 and preeclampsia.