It has been widely reported that glomerular TRPC6 channels are substantially more abundant in type 1 and type 2 diabetes and in podocytes cultured in the presence of elevated external glucose.28, 29, 30, 31, 32, 33 This is due at least in part to oxidative stress that can be driven by hyperglycemia, and by the surrounding pro‐inflammatory milieu.1 In addition, a protective effect of Trpc6 knockout has been reported in animal models of type 1 diabetes, although the outcomes varied substantially depending on which animal model was used. The gene discussed is TRPC6; the disease is type 2 diabetes mellitus.