However, when mice with specific inactivation of JAM-A in endothelial and hematopoietic cells (Tie-2-Cre-JAM-A−/−mice) (68) were treated with DSS, resulting colonic inflammation was comparable to controls and much less severe than in JAM-A KO mice, strengthening the hypothesis of a primary defect of epithelial origin that leads to colitis (69). This evidence concerns the gene F11R and colitis.