The complete correspondence between the site of preferential adduct binding detected in HCV-HCC cases with those observed hepatocytes in vitro treated with a ROS-generating system, e.g., the xanthine plus xanthine oxidase system [20], as well as with an over-represented mutational profile, e.g., the codon 176, in HCV-HCC tumors [24], strongly indicates that oxidative stress and ROS potentially produced during viral infection and inflammatory processes can be behind the high rates of G:C to T:A transversions and G:C to A:T transitions in HCV-HCC tumors [24]. This evidence concerns the gene XDH and hepatocellular carcinoma.