In Gnai2−/− mice developing spontaneous inflammatory bowel disease, gut-derived T cells from Rgs1−/− mice displayed increased chemotaxis to CXCL12, suggesting that the balance between expression of Gαi2 and RGS1 in gut T cells may control their retention within the gastrointestinal mucosa. This evidence concerns the gene CXCL12 and inflammatory bowel disease.