A most significant finding from this study was that compared to either ACE2 or Mas KO mice, mice with double deletion of ACE2 and Mas genes developed more severe hypertension and hypertensive nephropathy including higher levels of blood pressure and serum creatinine, a significant fall of creatinine clearance, and progressive renal inflammation and fibrosis. The gene discussed is MAS1; the disease is hypertensive nephropathy.