Myofibroblasts also form electrical coupling (through connexin) with cardiomyocytes in the heart.41 Existing myofibroblasts may actively contribute to the structural and electrical remodelling leading to the development of cardiac arrhythmias.9 Therefore, a novel antiarrhythmic therapeutic approach targeted at the CF population is needed.40, 42 We tested the expression of myofibroblasts using a specific marker α‐SMA in vitro. The gene discussed is ACTA1; the disease is chronic obstructive pulmonary disease.