Pathophysiologically, chronic hepatic injuries initiate the production of various fibrogenic cytokines in liver tissue, and the continued production of fibrogenic cytokines, such as transforming growth factor-beta (TGF-β), connective tissue growth factor (CTGF), and platelet-derived growth factor (PDGF), causes the transdifferentiation of quiescent nonparenchymal hepatic stellate cells (HSCs) into fibrogenic myofibroblast-like cells [8]. This evidence concerns the gene CCN2 and hepatotoxicity.