Deeper mechanistic studies have revealed that during the late phase of RSV infection, high mobility group box 1 (HMGB1) forms a complex with CXCL12 and specifically recruits natural killer (NK) cells to the airways via the CXCR4 receptor, significantly exacerbating persistent airway inflammation and airway hyperresponsiveness (AHR). This evidence concerns the gene CXCL12 and airway hyperresponsiveness.