In addition, the activation of NLRP3 inflammasome in monocytes infiltrating the lamina propria and M1 pro-inflammatory macrophages isolated from intestinal specimens of IBD patients, seems to contribute to the disruption of epithelial barrier through a deregulation of tight junction proteins (i.e., claudin-1, claudin-2, and junctional adhesion molecule-A), as well as to induce epithelial cell apoptosis (76). Here, F11R is linked to inflammatory bowel disease.