To date, the exact etiology of preeclampsia remains unknown. However, evidence obtained in recent years, supports the theory that angiogenic imbalance is the end common pathway that leads to clinical preeclampsia. During normal pregnancy, vascular endothelial growth factor (VEGF) and placental growth factor (PlGF) promote pro-angiogenic state that regulates vascular tone and glomerular capillary health. In preeclampsia, these proteins are antagonized by excessive placental production of soluble fms-like tyrosine kinase-1 (sFlt-1), thereby creating angiogenic imbalance. After delivery, this imbalance resolves within hours to days correlating with the resolution of the disease. One of the observations that marked sFlt-1 as key player in the pathogenesis of preeclampsia was made in an animal model. It was demonstrated that preeclampsia can be induced in animal model by over expressing sFlt-1 alone. In their model hydrophilic statins treatment decreased sFlt-1 levels and up-regulated VEGF and PlGF levels. Most importantly, statins ameliorated preeclampsia symptoms by improving hypertension and proteinuria in the preeclamptic mice.