More recent evidence has suggested dysregulation of wild-type TRPC6 channels in acquired glomerular diseases [10] and in in vitro models in which podocytes are exposed to serum or plasma samples from patients with recurrent focal and segmental glomerulosclerosis (FSGS) or factors implicated in the pathogenesis of primary FSGS [11,12]. Here, TRPC6 is linked to focal segmental glomerulosclerosis.