Mutations in transient receptor potential canonical 6 (TRPC6) channels and polycystin-2, a prototypical member of a subfamily of the TRPC channel superfamily, have been reported to cause familial focal segmental glomerulosclerosis and autosomal dominant polycystic kidney disease, respectively [36–41]. This evidence concerns the gene TRPC6 and autosomal dominant polycystic kidney disease.