In preeclampsia, elevated circulating levels of cellular and sub-cellular placental debris, including shedding of syncytiotrophoblast membrane fragments [1], [3], cell-free fetal DNA [46] and soluble fms-like tyrosine kinase 1 (sFlt-1) [47], have been shown to induce endothelial damage and precede onset of the clinical syndrome. Here, FLT1 is linked to preeclampsia.