Treatment with carbon tetrachloride (CCl4) in Tβ4-overexpressing transgenic mice significantly upregulates the expression of linked protein kinase (ILK) and increases the phosphorylation of GSK-3β, which produced inactive GSK-3β, thereby promoting HSC activation and transdifferentiation and excessive collagen accumulation, ultimately resulting in liver fibrosis. Here, GSK3B is linked to Hepatic fibrosis.