Glomerulosclerosis as ascertained by light microscopic histology in the albumin overload model is minimal, at least on the Sprague Dawley background, and therefore the experimental design did not allow us to ascertain if TRPC6 inactivation can exert a glomeruloprotective effect similar to those that occur during anti-GBM glomerulonephritis [21], in aging [22], and in chronic PAN nephrosis [18]. The gene discussed is TRPC6; the disease is glomerulosclerosis.