Based on our data, we postulate that the reduction of HDAC2 expression as well as HDAC activity not only directly enhances the expression of inflammatory genes, but may account for the activation of NF-κB and cause the expression of inflammatory mediators in COPD patients, which may be a potential mechanism for the pathophysiology of COPD. Here, NFKB1 is linked to chronic obstructive pulmonary disease.