Taken together, (i) the increase of tubular p21 expression in diabetic patients with DKD, but not in diabetic patients without DKD, (ii) the increase of urinary p21 in diabetic patients in association with an increasing KDIGO grade of CKD, and (iii) the persistent increase of urinary p21 despite improved blood glucose levels in diabetic patients support a model in which renal tubular p21 expression reflects persistent tubular damage in DKD, contributing to the hyperglycemic memory. This evidence concerns the gene CDKN1A and diabetic kidney disease.