NOD2 and Crohn disease: Although the exact mechanisms by which these mutations lead to disease is still not clear; data indicate that these mutations impair the mucosal barrier function due to a deficiency in bacterial clearance and activation of toll‐like receptors and Th1 immune responses.54, 57 Recent studies suggest that these defects may also alter the recognition of endoplasmic reticulum stress‐induced NOD1/NOD2 activation and further contribute to the development of Crohn's disease.24, 54