The present findings demonstated that (1) Ang II-stimulated ER stress contributes to endothelial dysfunction; (2) Ang 1–7 inhibits Ang II-stimulated ER stress and is most likely mediated via Mas receptor and (3) Ang 1-7-induced inhibition of ER stress augments NO bioavailability and thus restores the impaired EDR. The gene discussed is ANGPT1; the disease is endothelial dysfunction.