OSMR (oncostatin M receptor) is a type I cytokine receptor that functions as a coreceptor in the IL-31 signaling pathway and as a cognate receptor for oncostatin M (OSM). OSMR associates with IL31RA or LIFR and GP130 on the cell surface to transduce cytokine signals 1. Upon OSM binding, OSMR activates STAT3 and MAPK signaling cascades 23, driving diverse cellular responses including proliferation and inflammatory programs. OSMR mediates critical pathophysiological processes across multiple tissues. In glioblastoma, macrophage-derived OSM engages OSMR to promote mesenchymal transition via STAT3 activation 1. In cancer cachexia, OSM-OSMR signaling induces muscle atrophy through JAK/STAT3 pathway activation and upregulation of atrophy genes like Atrogin1 24. OSMR is also implicated in inflammatory bowel disease, where high OSM/OSMR expression in intestinal stromal cells correlates with disease severity and predicts anti-TNF therapy failure 5. Additionally, OSMR expansion in human dorsal root ganglion nociceptors links OSM signaling to neuropathic pain through MAPK-dependent neuronal activation 3. In lung cancer, exosomal upregulation of OSMR promotes macrophage polarization and metastasis 6. Therapeutic targeting of OSM-OSMR signaling shows promise for treating muscle wasting, IBD, and potentially neuropathic pain.