A lot of studies have shown the key role of cyclin-dependent kinase inhibitor (CDKI) such as p21 and P27 in MC hypertrophy [5–7]; attenuation of p21 by antisense oligodeoxynucleotide (ODN) could decrease MC hypertrophy induced by hyperglycemia and IGF-1 [8]; as a result diabetic p21 −/− mice did not develop glomerular hypertrophy; all data suggest p21 may be necessary for glomerular hypertrophy mediated by TGF-β1 in chronic renal diseases including DN [5, 9]. This evidence concerns the gene CDKN1A and liver dysplastic nodule.