No experimental model reproduces exactly human liver fibrosis by etiology. Nonetheless, each of the models reviewed in this article has served to enhance our understanding of pathogenetic mechanisms of liver fibrosis. There have been important common findings derived from several different models. The best example is the role of Ito cells in liver fibrogenesis. Involvement of Ito cells was consistently seen in the experimental models regardless of whether the fibrogenic stimulus was nutritional, hepatotoxic, or immunologic. Cellular and molecular mechanisms of Ito cell activation have begun to be explored in different models. Another example is the role of TGF beta in liver fibrogenesis. In both murine schistosomiasis model and Tsukamoto-French rat model, TGF beta was shown to be closely associated with fibrogenesis. With both in vitro and in vivo experimental approaches using cellular and molecular techniques, the experimental model of liver fibrosis will continue to provide data on the pathogenetic mechanisms of liver fibrogenesis. Future genetic and molecular approaches may allow development animal models with liver fibrosis that is inducible and genetically similarity to that of man.