Consistently, we found that knockout of OTUD4 in IECs increased the phosphorylation of TAK1, p65 and p38 after DSS treatment or S.t. infection (Fig. 5C), indicating that OTUD4 restricts the activation of NF-κB and MAPKs in IECs during gut inflammation or bacterial infection. The gene discussed is NFKB1; the disease is bacterial infectious disease.