These changes resulted in increased expression of proinflammatory cytokines, such as IL-17A and IL-22,10,37 and mucosal sIgA antibody,34,36 that further led to the production of antimicrobial peptides such as CRAMP, β-defensin-1, and β-defensin-3, consequently leading to inflammatory diseases like IBD.10 This evidence concerns the gene CAMP and inflammatory bowel disease.