MRP8/14 induces sustained IP-10 production by activating the IFNβ-JAK1/TYK2-STAT1-IRF7 pathway, which subsequently attracts numerous CXCR3+ T cells and results in an exaggerated inflammatory response and lung injury in the context of endotoxemia. The gene discussed is STAT1; the disease is serum lipopolysaccharide activity.