Oxidative stress drives COPD through the activation of several mechanisms, including the proinflammatory transcription factor nuclear factor-KB (NF-κB) [30], the p38 mitogen-activated protein kinase (MAPK), the generation of autoantibodies to carbonylated proteins, the reduced expression of sirtuin-1 and histone deacetylase HDAC2, DNA damage, the reduced activity of antiproteases and the increased release of transforming growth factor (TGF)-β, as well as lipid peroxidation products such as malondialdehyde (MDA). This evidence concerns the gene HDAC2 and chronic obstructive pulmonary disease.