This could actually be relevant at several levels through the release of extracellular AGR2 which might as previously found in other models induce Epithelial‐to‐Mesenchymal Transition markers13 to promote fibrosis which is a hallmark of Crohn's disease and in the mean‐time to promote the recruitment of macrophages to the site of damage to precondition the tissue for uncontrolled inflammation. Here, AGR2 is linked to Crohn disease.