The pathogenesis of the pregnancy complication preeclampsia remains incompletely resolved. Nevertheless, defective remodeling of the maternal vessels supplying nutrients and oxygen to the placenta is recognized as the root cause in most (all) cases (1). Furthermore, the translation of this reduced perfusion into the maternal syndrome, diagnosed by increased blood pressure and proteinuria but consisting of multisystemic organ dysfunction, involves abnormal function of vascular endothelium (2). The clinical changes of preeclampsia are reversed when the placenta is delivered. Several years ago, these findings led Karumanchi and his group (3) to search for aberrant expression of angiogenic and antiangiogenic factors in placentas of women with preeclampsia. Angiogenic factors both stimulate angiogenesis and appear necessary for maintenance of endothelial health and integrity (4). In 2003, the Karumanchi group (3) reported that the placentas of women with preeclampsia strikingly over express a soluble receptor for the angiogenic factors, vascular endothelial growth factor (VEGF) and placental growth factor. The soluble receptor, soluble fms-like tyrosine kinase (sFlt1) acts as an antagonist of VEGF and placental growth factor by binding and sequestering these growth factors from interaction with their receptors Flt1 and Flk1. They also demonstrated that the circulating concentration of sFlt1 was strikingly elevated in pregnancy and even more so in preeclampsia. Furthermore, overexpressing this receptor in rats resulted in a preeclampsia-like syndrome (3). Subsequently, it was found that sFlt1 was increased weeks before clinically evident preeclampsia, supporting a role in pathogenesis and raising the hope for a predictor of preeclampsia (5). sFlt was originally identified as 90-to 100-kDa glycosylated protein, a product of a splice variant of the Flt1 gene (6). Recent studies have provided evidence for the presence of additional transcripts that are different in their 3! sequences (7). At the protein level, sFlt variants that are different in antigenicity and peptide length from the original sFlt have been identified in plasma samples of normal and preeclamptic women and released from placental explants (8).