In a carbon tetrachloride–derived liver inflammation model, Yao et al. [53] blocked GSK-3β with wortmannin and pre-treated mice with anti-IL-10 antibody, which abolished the beneficial effects of MRS and raised the levels of phosphorylated NF-κB and MAPK proteins supporting the involvement of these pathways in the anti-inflammatory effects of CH4. The gene discussed is GSK3B; the disease is Hepatitis.