We propose that increased OSM signaling allows activated STAT3 to hijack SMAD3 into a STAT3/SMAD3 complex that shifts the equilibrium away from the SMAD3/IRF7 complex, thereby converting SMAD3 from a tumor suppressor, capable of activating IFN-β, into a tumor promoter that activates a mesenchymal/CSC program. The gene discussed is IRF7; the disease is neoplasm.