Studies conducted in experimental animal models of diabetes (streptozotocin‐induced diabetes and db/db mice) have shown a sustained activation of UPR, with increased levels of phosphorylated PERK, eIF2α and CHOP, with activation of ATF6 and caspase with secondary glomerular and tubular cells apoptosis.55, 56, 57. Here, ATF6 is linked to diabetes mellitus.