In these experiments, we used Sprague‐Dawley rats in which TRPC6 channels were inactivated by a global constitutive deletion in exon 2 of the Trpc6 gene generated by CRISPR/Cas9, which we have described previously.25 Rats homozygous for this deletion, hereafter referred to as Trpc6del/del, exhibited marked protection from chronic PAN nephrosis compared to wild‐type littermate controls (Trpc6wt/wt),25 and we hypothesized that these animals would also be protected from STZ‐induced nephropathy. The gene discussed is TRPC6; the disease is kidney disorder.