Moreover, TRPC6 knock-out in mice or rats confers protection to the development of experimental diabetic nephropathy, puromycin aminonucleoside (PAN)-induced nephrosis and Angiotensin II-induced glomerular hyperfiltration [6,7,8] Enhanced Ca2+ influx via TRPC6 has been shown to be detrimental to podocytes as manifested by cytoskeletal rearrangements and subsequent podocyte death [9,10,11]. Here, TRPC6 is linked to nephrosis.