However, the data presented here suggest that defective RAGE signaling contributes to the development and progression of airway remodeling in the absence of Th2/Th17-mediated granulocytic inflammation Given that we identified HMGB1 as a central mediator in the pathogenesis of airway remodelling, our findings suggest that anti-HMGB1 therapy may be a novel therapeutic for the treatment of asthma, irrespective of inflammatory cell subtype. The gene discussed is HMGB1; the disease is asthma.