Oxidative stress is associated with the pathogenesis of COPD through mechanisms including the oxidation of arachidonic acid to isoprostanes, which cause bronchoconstriction and release of plasma exudate [20] Furthermore, by modifying carcinogens into active, mutagenic metabolites, NQO1, CYP1B1 and EVL have been implicated in the pathogenesis of human tumours [27], [46]. This evidence concerns the gene EVL and chronic obstructive pulmonary disease.