Not surprisingly, C3G inhibited NF-κB phosphorylation, reduced mRNA expression of pro-inflammatory cytokines including IL-1β, IL-6, IL-8, COX-2, and TNF-α, and protein levels of apoptosis related genes in DSS-induced colitis mice, providing new ideas for using C3G as adjuvant agent for treating UC [68]. The gene discussed is TNF; the disease is colitis.