In support of this possibility, (1) insulin signaling was impaired in TRPC6 knockout podocytes compared to wild type podocytes [135], and (2) previous studies by Welsh et al. [136] found that podocyte specific knockout of the insulin receptor caused heavy proteinuria and histopathologic features of diabetic kidney disease in the normoglycemic environment. The gene discussed is TRPC6; the disease is diabetic kidney disease.