What’s more, sulfasalazine significantly decreased the expression of pro-inflammatory cytokines, such as TNF-α and IL-6, as well as TLR4 activation in colon tissue compared with DSS-treated mice, indicating the effective but not satisfactory enough effect of sulfasalazine in UC treatment, which was consistent with the utilization status of sulfasalazine in IBD patients. The gene discussed is TLR4; the disease is inflammatory bowel disease.