Multiple factors have been implicated in the pathogenesis of DN including hyperglycemia induced activation of advanced glycation end products (AGEs) and reactive oxygen species (ROS); JAK-STAT pathways and G protein signaling; activation of the PKC, renin-angiotensin aldosterone system (RAAS), transforming growth factor β-Smad-mitogen-activated protein kinase (TGF-β-Smad-MAPK), deregulated expression of cyclin dependent kinases (CDK), and their inhibitors; and aberrant expression of ECM proteins, ECM-degrading enzymes, metalloproteinases, and their inhibitors [8]. Here, TGFB1 is linked to liver dysplastic nodule.