Taken together with our findings that H2O2 did not affect IL-32 expression alone but did augment IFNγ-induced IL-32 expression, IL-32 could be induced higher in airways of COPD patients who have increased oxidative stress under the exacerbation caused by viral infection and/or an inflammatory condition in which CD8+ T cells are activated. The gene discussed is CD8A; the disease is viral infectious disease.