However, these over expressing point mutations models (E896K and P111Q), as well as the overexpression of wild-type Trpc6, showed the disadvantage of presenting a kidney disease of late onset (5-9 months) making them an expensive tool for investigating the mechanisms involved in the pathogenesis of FSGS due to mutations in Trpc6. Here, TRPC6 is linked to focal segmental glomerulosclerosis.