Potentially, XN may target fibrosis, cirrhosis, and HCC associated with chronic HCV infection because of the anti-fibrotic effects, brought on by the inhibition of hepatic TGF-β1 expression, and because of XN-induced inhibition of NF-κB-mediated inflammation, cancer, and the reduction of hepatic inflammation, steatosis, and fibrosis in HCV-infected Tupaias [174]. This evidence concerns the gene NFKB1 and Cirrhosis.