It is thought that inadequate remodeling of the maternal spiral arterioles by the extravillous trophoblast generates periodic placental malperfusion, leading to oxidative and endoplasmic reticulum stress.1, 3, 4 This causes increased placental release of anti-angiogenic factors such as soluble fms-like tyrosine kinase-1 (sFLT1)5 and soluble endoglin (ENG).6, 7 This leads to maternal endothelial dysfunction, which then causes hypertension and systemic organ injury.8 The gene discussed is ENG; the disease is Hypertension.