Key systems, including the RAAS, the SNS, and vasopressin, drive volume expansion and arterial and venous vasoconstriction, which are also core contributors to the progression of CHF[50,51], The dysregulation of the RAAS Activated by low renal perfusion or increased sympathetic activity[52], RAAS leads to the release of renin, which converts angiotensinogen to angiotensin I, and ACE further converts this to angiotensin II. The gene discussed is AGT; the disease is congestive heart failure.