MMP-2 accelerates the development of early CKD because it can degrade the basement membrane, destroy the glomerular filtration membrane, activate TGF-β1, and promote the phenotypic transformation of tubular epithelial cells [9]; renal tubular atrophy, renal fibrosis, and excessive ECM deposition in the basement membrane and interstitium are observed in advanced CKD, suggesting that MMP-2 activity is insufficient at this stage [10]. The gene discussed is TGFB1; the disease is renal fibrosis.