vascular remodeling, and atherosclerosis (7, 8, 9). Because of the adverse cardiovascular effects of RAS upregulation, its inhibition through ACE inhibitors, angiotensin II receptor blockers (ARBs), and mineralocorticoid receptor antagonists (MRAs) has been critical for the management of various cardiovascular diseases. In the last 2 decades, the identification of ACE2 and its involvement in the counter regulation of the classic RAS has