Alternatively, oxidants oxidize the cysteine residue in Keap‐1 to prevent it from binding to Nrf.19 Through these means, Nrf is free to translocate to the nucleus and induce the expression of antioxidant genes.20 Therefore, the ability of Nrf2 to regulate antioxidant and antiinflammatory response could be a mechanism for the regulation of the pathogenesis of COPD. This evidence concerns the gene NKRF and chronic obstructive pulmonary disease.