TRPC6 and focal segmental glomerulosclerosis: Studies on secondary FSGS found that TRPC6-originating calcium influx leads to the abnormal localization of Nephrin in the SD, such that Nephrin is unable to function normally, leading to changes in TRPC6-mediated calcium currents, which are critical in the regulation of intracellular molecules and cytoskeletal behavior in podocytes [49, 50].