These include, (i) empiric antibiotic therapy experiences has been satisfying in certain IBD patients [109], (ii) IBD patients have enhanced concentrations against indigenous commensal bacteria [110], (iii) genetic deviants that are consociated with bacterial spotting, such as NOD2 [111], and T cell immunity, such as IL23R, are incriminated in IBD [112] and (iv) most animal model studies of colitis require commensal bacteria for the initiation or trigger of intestinal inflammation [113]. Here, IL23R is linked to inflammatory bowel disease.