TNF, an important inflammatory factor involved in the pathogenesis of IBD, not only collaborates with IL-23 to initiate the production of pathogenic IL-17 by ILC3s, but also induces chemokine expression that attracts neutrophils, including CXCL1, CXCL2, and CXCL5, which synergizes with IL-17A to further recruit neutrophils to release tissue damage mediators, resulting in exacerbation of intestinal epithelial cell apoptosis and tissue damage (106). This evidence concerns the gene TNF and inflammatory bowel disease.