The pathogenesis of preeclampsia remains incompletely elucidated, however increased attention has been directed toward the role of angiogenic and antiangiogenic factors including elevated soluble fms-like tyrosine kinase 1 (sFlt1) and soluble endoglin (sEng, a receptor for members of the TGFβ superfamily), and lower placental growth factor (PlGF) [5], [6], [7], [8]. This evidence concerns the gene ENG and preeclampsia.