Clinical evidence has indicated a loss in nephrin and ZO-1 expression in glomerular podocytes, whereas desmin, FSP1, MMP-9, and key EMT regulators, such as Snail and integrin-linked kinase (ILK), expression were significantly increased in DN patients [37–39], suggesting an active EMT formation in podocytes after DN. The gene discussed is ILK; the disease is liver dysplastic nodule.