The second is the cyclin-dependent kinase inhibitor 2B antisense RNA 1 (CDKN2B-AS1) that promoted fibrosis via transforming growth factor-β (TGF-β) signaling [32], which, in turn, increased the synthesis and deposition of extracellular matrix, eventually causing glomerulosclerosis and tubulointerstitial fibrosis in DN [11]. This evidence concerns the gene TGFB1 and liver dysplastic nodule.