During early pregnancy, abnormal placental implantation elicits uteroplacental hypoxia, which decreases proangiogenic PlGF expression and elevates antiangiogenic sFlt-1 and sEng production through stabilization of the HIF-1α protein, consequently leading to trophoblast and endothelial dysfunction, spiral artery abnormalities, and glomerular injury1. This evidence concerns the gene HIF1A and endothelial dysfunction.