First of all, as Mahler et al1described in the introduction to the article, the pathogenesis of COPD consists of several mediators other than IL-8. Target molecules in COPD involve tumor necrosis factor, interferon-γ, and IL-6 as cytokines, CCL2, CCL3, and CCL13 as chemokines, and several proteinases such as matrix metalloproteinase and neutrophil elastase.2–3 Thus, only IL-8 blockade itself may not have a great influence on disease activity. We are also concerned about the relatively low circulatory levels of the cytokine (ie, < 50 pg/mL) in the subjects examined. Alternatively, these data may indicate that IL-8 does not contribute to the symptoms of COPD in stable stages of the disease. Instead, we want to be informed of any previous studies in the literature in which the possible correlations between IL-8 and an exacerbated phase of COPD have been demonstrated.