Indeed, our finding that stimulation with TGF-β of primary cultured fibroblasts derived from nasal polyps elevated the α-SMA expression from 31.0% to 94.1% and enhanced fibronectin production, supports the role of TGF-β in the enhancement of myofibroblast differentiation and ECM production , possibly forming a fibrotic wall as a defensive mechanism to prevent edema and inflammation from spreading. The gene discussed is ACTA1; the disease is nasal cavity polyp.