Decreased expressed HDAC2 have been noted both in severe COPD and uncontrolled asthma, and abolishes the effect of glucocorticoids by keeping glucocorticoid receptor from deacetylation and unable to form a protein–protein complex that represses the NF-κB pathway [59,60,61]. This evidence concerns the gene NFKB1 and chronic obstructive pulmonary disease.