It has been suggested that increased renin-angiotensin system (RAS) activation and elevated levels of angiotensin II, frequently observed in patients with diabetes, lead to TRPC6 activation with subsequent increased intracellular calcium (Ca2+) influx and increased podocytes apoptosis (123); moreover, deletion of TRPC6 in diabetic mice preserves renal histology and prevents albuminuria (122). Here, TRPC6 is linked to diabetes mellitus.