Myofibroblasts that express alpha-smooth muscle actin (α-SMA) comprise an activated cell phenotype of fibroblasts with a high capacity for ECM protein secretion and play an important role in ECM remodeling of many pathologic conditions of the human airway, including asthma, chronic rhinosinusitis, and nasal polyps [7, 8]. The gene discussed is ACTA1; the disease is nasal cavity polyp.