While the TRPC6-mediated Ca2+ entry was found to contribute to migration and invasion, the gain-of-function mutation of TRPC6 found in several podocytes leads to focal and segmental glomerulosclerosis (FSGS), a leading cause of glomerulonephritis and chronic kidney disease [46,47] and proteinuria [48] due to alteration of actin organization and subsequently cell migration repression. The gene discussed is TRPC6; the disease is glomerulonephritis.