The angiotensin II links to the AT1 receptors, and this causes vasoconstriction, fibrosis, and pulmonary oedema, so that the down regulation of the ACE2 would reduce the synthesis of the angiotensin 1–7, which has some opposite effects: vasodilatation, antifibrotic, and antiproliferative. The gene discussed is AGT; the disease is pulmonary edema.