Among these, sFlt1 can cause endothelial dysfunction in the maternal blood vessels by binding vascular endothelial growth factors and placental growth factor [4]; AT1-AA can react with the AT1 receptor in a stimulatory fashion similar to angiotensin II signalling, which could contribute to maternal hypertension [6]; MBG, involved in the pathogenesis of preeclampsia, has been demonstrated to cause hypertension, proteinuria, and intrauterine growth restriction in the rat model of preeclampsia [8]. Here, AGTR1 is linked to fetal growth restriction.