However, inhibition of the JAK pathway continued to inhibit expression and production of CXCL9, CXCL10 and CXCL11 in the presence of TNFα, indicating that inhibition of STAT-1 phosphorylation is an essential regulatory step in this process and indicates that JAK inhibition may be a good therapeutic approach in COPD where multiple inflammatory mediators interact. Here, CXCL9 is linked to chronic obstructive pulmonary disease.