Although animals studies have shown that activation of AT1-AA is associated with elevation of intracellular Ca2+ in vascular smooth muscle cells[11], stimulation of placental and vascular NADPH oxidase[12] and activation of NF-κB[13], all of which may cause inflammation and contribute to pathogenesis of preeclampsia via AT1-AA, there is less specific data to show whether AT1-AA is elevated in patient with EOC and correlated with the advanced progression of EOC. Here, AGTR1 is linked to preeclampsia.