Either as a direct cause of focal segmental glomerulosclerosis (FSGS) caused by the gain-of-function mutation in transient receptor potential cation channel member 6 (TRPC6) [9] or as a uniform response to stress in this cell type, e.g., in protamine sulfate nephropathy [10] or in complement C5b-9 complex-mediated podocyte injury [11]. This evidence concerns the gene TRPC6 and focal segmental glomerulosclerosis.