Oxidative stress is also elevated due to defects in redox defense mechanisms involving glutathione (GSH), catalase, or superoxide dismutase (SOD), which induces several events related to NASH and carcinogenesis, including DNA damage, tissue remodeling, and alterations in gene expression such as mutations in the p53 tumor suppressor gene, which is observed in HCC [169,170]. This evidence concerns the gene TP53 and hepatocellular carcinoma.