Taken together, defects of autophagic activity as the result of mutations in autophagy-associated genes (i.e., ATG16L1 and IRGM) and bacterial sensors (NOD2) have been associated with the impaired clearance of harmful bacterial species associated with Crohn's disease, impaired antigen presentation, and also with the higher production of proinflammatory cytokines implicated in the pathogenesis of Crohn's disease. This evidence concerns the gene NOD2 and Crohn disease.