Next, ATG16L1, a gene identified by GWAS studies as IBD risk gene, regulates the development of T cells and cell autophagy.76 In mouse models, deletion of ATG16L1 triggers spontaneous intestinal inflammation with severely reduced CD4 + T cells.77 In ATG16L1 homozygous CD patient’s, enrichment of Fusobacteriaceae, Bacteroidaceae, Enterobacteriaceae in ileal tissue was observed as compared to control patients.63 Fucosyltransferase 2 (FUT2), an enzyme that regulates intestinal epithelial cells-microbe interaction is another factor that lost was found to increase susceptibility to CD development. This evidence concerns the gene FUT2 and inflammatory bowel disease.