ACE converts circulating Ang I to Ang II (Renin-Angiotensin system; RAS) and also degrades bradykinin, an NO inducer, and is responsible for an increase in ROS, vasoconstriction, inflammation, and fibrosis as well as ECM dysregulation representing current targets in designing therapeutic to combat CKD progression [32,33,34]. Here, AGT is linked to chronic kidney disease.