In contrast, HAS1 and HAS3 upregulation after HSC activation are not as dramatic.4 HSCs are responsible for HAS2 expression and HA production in liver fibrosis in a study of mice lacking HAS2 expression in their HSCs.4 Mice lacking HAS2 expression in their HSCs exhibit reduced HSC activation and fibrosis, along with abolished HA deposition in the liver and no upregulation of circulating HA compared with baseline. This evidence concerns the gene HAS2 and Hepatic fibrosis.