The pathophysiological mechanism underlying the increased ROS production which is invariably present in all forms of CKD is at least partly mediated by the pathological upregulation of the intrarenal angiotensin system, as evidenced by marked upregulation of angiotensin II receptors (AT1 and AT2) and simultaneous increases in angiotensin II-producing cells in the diseased kidney. The gene discussed is AGT; the disease is chronic kidney disease.