Progressive tissue remodeling characterized by extensive collagen production and excess extracellular matrix deposition leads to intestinal fibrosis and stricture formation in patients with fibrostenotic Crohn’s disease. Currently medical therapies can delay but not prevent the development of critical fibrostenosis necessitating surgery. Endoplasmic reticulum (ER) stress and activation of the unfolded protein response (UPR) are associated with intestinal epithelial cells damage and apoptosis in Crohn’s disease.