Oncostatin M (OSM) is a highly expressed cytokine in IBD and high pretreatment expression is strongly associated with failure of anti-TNF-a therapy. OSM promotes intestinal inflammatory pathology and genetic deletion or pharmacological blockade of OSM significantly attenuates colitis in mice. Our hypothesis is that OSM acts as an inflammatory amplifier and driver of disease chronicity by impacting on both stromal and epithelial cells. We believe that a better understanding of OSM-OSMR pathway in intestinal biology could facilitate the development of novel therapeutic strategies targeting this pathway in IBD.