Given the established heterogeneity between CD and UC with respect to location, inflammation penetrance (transmural vs. mucosal), cytokine profiles, unique vs. overlapping genetic risk variants, and most pertinently the differential responses to various treatment approaches (i.e., anti-TNF to treat CD; the pan JAK inhibitor, tofacitinib, to treat UC), it should not be surprising that lubiprostone also displayed a selective effect between IBD subtypes [42]. This evidence concerns the gene TNF and irritable bowel syndrome.