The failure of ACE2 to do so allows ACE to act on the Ang I and release Ang II which, after binding with AGTR1, induces various deleterious effects including apoptosis, inflammation, vasoconstriction, hypertension, cardiac hypertrophy, collagen production, reactive oxygen species by overproduction of TGF-β, and expression of ICAM-1, VCAM-1, and MCP-1 (2). Here, AGT is linked to cardiac hypertrophy.