We confirmed the fibrotic phenotype was induced by TGF-β1 by hepatocellular injury (decrease in albumin staining and increased miR-122-5p release) and by HSC activation and ECM deposition (increased αSMA and FN1 staining) in primary cells, FN1 being a crucial ECM component produced alongside Col I during liver fibrosis progression [2]. Here, ACTA1 is linked to Hepatic fibrosis.