ACE inhibition has potential anti-fibrotic effects in murine models of unilateral ureteral obstruction and progressive renal fibrosis [21] as well as in diabetic mice by inhibiting hyperglycemia-induced growth factor production and subsequent fibroblast activation [22]; however, other mechanisms can contribute to the development of renal fibrosis in diabetic patients, and it is unknown whether ACE inhibitors or other novel drugs such as SGLT-2 inhibitors may modulate these processes. Here, ACE is linked to renal fibrosis.