However, airway fibrosis is driven by myofibroblasts (an α smooth muscle actin (αSMA) positive fibroblast subtype), and recently an αSMA-positive fibroblast subtype was identified in the lung parenchyma, with approximately three times more αSMA-positive cells in the parenchyma of individuals with asthma compared to non-asthmatic control subjects [21, 22] suggesting that parenchymal-derived fibroblasts in asthmatics may play a role. This evidence concerns the gene ACTA1 and fibrosis.