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. This evidence concerns the gene COL1A2 and Hepatic fibrosis.