It was also found that IL-17A is overexpressed in CD strictures compared with non-structured CD areas and gut control [40], and that IL-17A is increased in the inflamed areas of patients with IBD [41], and has a role in epithelial permeability independent of IL-23 [42], further confirming the role of IL17A in the pathogenesis of CD. This evidence concerns the gene IL17A and inflammatory bowel disease.