A recent study showed that adverse pregnancy outcomes such as fetal growth restriction (FGR), placenta previa, placental abruption and pre-eclampsia were associated with increased serum levels of soluble fms-like tyrosine kinases (sFlt-1), 8-epi-prostaglandinF2-alpha (8epi-PGF2α) and decreased levels of the placental growth factor (PlGF) and of total antioxidant capacity (TAC), in addition to vascular endothelial damage, cardiovascular complications and an exaggerated inflammatory response [8, 9]. The gene discussed is PGF; the disease is fetal growth restriction.