It is well known that Ca2+ signalling in healthy podocytes is mainly mediated by angiotensin II and TRPC5 and 6 (nonselective cationic channels, downstream of angiotensin II signalling) [59]; interestingly, TRPC6 can play a dual role, as it has been shown that acute activation of this channel is able to protect podocytes from complement-mediated injury, while gain-of-function mutations/chronic hyperactivation can affect the SD and/or foot processes morphology leading to glomerular diseases, such as FSGS [60]. Here, AGT is linked to glomerular disorder.