Reduced levels of histone deacetylase-2 (HDAC2) have been observed in patients with COPD and refractory asthma [258,259], and one mechanism of reduced deacetylase activity is inactivation of HDAC2 by oxidative stress, which has been demonstrated in epithelial cells, animal models, and patients with COPD [260-262]. Here, HDAC2 is linked to chronic obstructive pulmonary disease.