In our study, we have investigated the liver expression levels of alpha-SMA (ACTA2) and of fibrillar collagen COL1A1, COL1A2, and COL3A1; of the pro-fibrogenetic cytokines TGFB1, TGFB2, PDGFB and IL-6-; as well as, the levels of the metalloproteinase inhibitors TIMP1 and TIMP2; and of the matrix metalloproteinanses, MMP2 and MMP9 in a model of liver fibrosis induced by repeated administrations of ConA to mice, resembling the course of AIH in patients poorly responsive to SOC treatment. The gene discussed is ACTA2; the disease is Hepatic fibrosis.