However, IL-36γ release from SAEC was detectable, and COPD SAEC released significantly more IL-36γ compared with nonsmoking controls (Figure 2D), suggesting that airway epithelial cells could be a major source of IL-36γ in peripheral airways, under basal conditions, and that these cells may be responsible for the elevated levels observed in BALF and nasal secretions in COPD. This evidence concerns the gene IL36G and chronic obstructive pulmonary disease.