Similarly, using the same DSS induced mouse model of colitis, we demonstrated that treatment of the mice with the PARK7/DJ-1 binging Comp23 improves the clinical symptoms, decreases the histological lesions, spleen enlargement, and the mucosal expression of IL-1β, IL-6, and IL10, and TGF-β of DSS-treated mice, suggesting the strong anti-inflammatory role of PARK7/DJ-1 and Comp23 (Figure 4). The gene discussed is IL1B; the disease is colitis.