There is increasing evidence that an imbalance between proangiogenic factors (e.g., vascular endothelial growth factor (VEGF) and placental growth factor (PlGF)) and antiangiogenic factors (e.g., soluble VEGF receptor-1 (sVEGFR-1) and soluble endoglin (s-Eng)) contributes to the pathophysiology of preeclampsia (PE) and IUGR. This evidence concerns the gene PGF and fetal growth restriction.