Clearance of p16-positive cells delayed the progression of diabetic kidney disease in STZ-induced INK-ATTAC transgenic mice, restored the levels of ATP, decreased the expression of the common SASPs, decreased glycolysis, and improved metabolic reprogramming of mitochondria, possibly through the AMPK and mTOR pathways (Fig. 9). This evidence concerns the gene CDKN2A and diabetic kidney disease.