Therefore, it is critical for regulating the actions of Ang II mediated by its AT1R. A previous study from our group showed that placental ACE2 mRNA expression was lower in pregnancies associated with fetal growth restriction (Delforce et al., 2019), suggesting that reduced placental ACE2 levels and reduced Ang-(1-7) production might contribute to the etiology of SGA. The gene discussed is AGTR1; the disease is fetal growth restriction.