Currently, elevated levels of soluble fms-like tyrosine kinase-1 and soluble endoglin, along with significantly reduced levels of placental growth factor, shift the balance in favor of antiangiogenic factors and induce microangiopathy in target organs such as the kidneys, liver, and brain, giving rise to preeclampsia [30,67,68]. The gene discussed is PGF; the disease is preeclampsia.