In COPD in vitro models of bronchial epithelial cells exposed to cigarette smoke extracts (CSE), Carbocysteine reduces oxidative stress, increases HDAC2 and HDAC3 expression inducing deacetylation processes, reduces pro-inflammatory markers (IL-8 mRNA, IL-8 release, Toll-like receptor-4 (TLR4) expression, lipopolysaccharide (LPS) binding) and inhibits neutrophil chemotaxis [33,34,35]. This evidence concerns the gene HDAC2 and chronic obstructive pulmonary disease.