Although complete mechanistic insight into the pathophysiology of preeclampsia remains elusive, one current model is that the disease is causally associated with elevated sFLT1 in the maternal circulation.3 It is hypothesized that increased placental release of sFLT1 results in elevated maternal serum levels of the protein, which then binds and inactivates PlGF in the maternal circulation, and it may also act directly on endothelial cells. The gene discussed is PGF; the disease is preeclampsia.