VIL1 and bacterial infectious disease: Consistently, knockout of OTUD4 in IECs promoted the K63-linked polyubiquitination of MyD88 and the activation of downstream NF-κB and MAPKs in inflamed IECs, and the inhibitor ST2825 for MyD88 inhibited the expression of AMPs both in Vil-Cre;Otud4fl/fl and in Otud4fl/fl intestinal organoids that were treated with LPS or PGN, or infected with S.t., indicating that MyD88 is the main target of OTUD4 in IECs in regard of AMP expression after DSS treatment or bacterial infection.