Furthermore, GRP78 is implicated in the development of diabetic kidney disease (DKD) and peritubular fibrosis in vivo since the administration of canagliflozin reduces ER stress impartment, protects proximal tubular cells, and restores subcellular localization of GRP78, SGLT2, and integrin-β1, reducing the fibrosis in DKD [74]. This evidence concerns the gene HSPA5 and diabetic kidney disease.