Placentas from anemia-affected pregnancies demonstrate abnormal vascular patterns and errant expression of angiogenic signaling molecules, including vascular endothelial growth factor, placental growth factor, and endothelial nitric oxide synthase.24 Similar derangements in angiogenesis have been identified in people with SCD,25 and these mechanisms could explain the increased rates of placentally mediated APOs, including HDP and intrauterine growth restriction, in deliveries among individuals with SCD and anemia in this study. The gene discussed is VEGFA; the disease is fetal growth restriction.