This reduced placental perfusion is associated with myriad changes [2–4] including imbalance between pro-angiogenic (e.g. vascular endothelial growth factor, VEGF) and anti-angiogenic (e.g. soluble fms-like tyrosine kinase-1, sFlt-1; soluble endoglin, sEng) factors in the maternal circulation [5], endothelial dysfunction, and endothelin pathway activation. Here, VEGFA is linked to endothelial dysfunction.