Previously, DNase-I was shown to protect mice from type-2 immunopathology33 and CS-induced acute airway inflammation,23 we further showed that the degradation of NETs-DNA by DNase-I treatment alleviated NF-κB-dependent cytokines and emphysema-phenotype in the long-term CS-treated mice, suggesting that DNase-I could offer modest protective effects against the sustained airway inflammation and subsequent alveolar destruction. The gene discussed is NFKB1; the disease is inflammatory response.