In diabetic (db/db) mice, antibody-mediated depletion of Tregs aggravated insulin resistance and exacerbated diabetic nephropathy, whereas, adoptive transfer of Tregs significantly improved insulin sensitivity and diabetic nephropathy by tipping the balance towards anti-inflammation and inhibiting CD8+ effector cell infiltration into the visceral adipose tissue (VAT) and kidneys. This evidence concerns the gene INS and diabetic kidney disease.