The recombinant human kallistatin treatment significantly reduced the expression levels of TGF-β1 and α-SMA in liver along with the progress of fibrogenesis in the rat model, indicating that the recombinant kallistatin had an inhibitory effect on hepatic fibrosis (Figure 1), at least partly via down regulation of the expressions of TGF-β1 and suppression of HSCs activation (Figure 3). The gene discussed is ACTA1; the disease is Hepatic fibrosis.