TRPC6 and focal segmental glomerulosclerosis: The involvement of loss-of-function TRPC6 mutations in the pathogenesis of FSGS indicates that, while elevated TRPC6-mediated Ca2+ influx in podocytes is detrimental for the kidney function, some basal level of TRPC6 activity may still be required for normal function of podocytes in the kidney glomeruli, especially in pediatric patients [264].