Oncostatin M (OSM) and OSM receptor (OSMR) were found to be highly expressed in inflamed intestinal tissue in patients with Crohn’s disease (CD) and ulcerative colitis (UC).1 West et al. also found elevations of mucosal OSM was strongly associated with treatment nonresponse to tumor necrosis factor-α inhibitors (anti-TNF).1 We hypothesized that increased abundance of plasma OSM would also be associated with anti-TNF nonresponse with our primary aim to identify an OSM cut-point for early anti-TNF nonresponse.