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. The gene discussed is ACTA1; the disease is chronic obstructive pulmonary disease.