Our previous study first showed that DACT1 was involved in atrial fibrillation (AF) [3], the most common cardiac arrhythmia in clinical practice, while also regulating the gap junction protein connexin 43 by accelerating cytoskeletal rearrangement via the accumulation of β-catenin in myocardial cells [3], which further suggests DACT1 might be a link between the cytoskeletal and gap junctions. This evidence concerns the gene DACT1 and chronic obstructive pulmonary disease.