Given the pathological role of the AGEs-RAGE axis in tubular cell apoptosis [12, 13, 17], blockade of insulin-induced SGLT2 overexpression may not just improve hyperglycemia by promoting urinary glucose excretion, but could also directly inhibit glucotoxicity to proximal tubular cells, thus protecting against tubulointerstitial damage in diabetic nephropathy. Here, INS is linked to diabetic kidney disease.