IL36G and chronic obstructive pulmonary disease: However, α-SMA, a myofibroblast differentiation marker, was significantly decreased in SAF from both nonsmoker and COPD subjects by both IL-36γ and IL-1α (Supplemental Figure 5C), suggesting that IL-36γ was driving these cells away from a myofibroblast phenotype to a potentially more proinflammatory and proteolytic state.