Therefore, identification of the GLP-1/GLP-1R axis and associated immunosuppression mechanism in human intestinal IELs will be critical to target intestinal inflammatory diseases, such as inflammatory bowel disease (IBD) or Crohn’s disease (CD) and coeliac disease, where IEL overactivation plays a significant factor in the pathogenesis [138–140]. This evidence concerns the gene GLP1R and inflammatory bowel disease.