It is well known that COPD has been associated with an increased incidence of AF,11–13 which is attributed to increased arrhythmogenicity from hypoxia,14 hypercapnia,15 pulmonary hypertension,16 ventricular remodeling,17 inflammation,18 and respiratory drug use.19 At a biochemical level, the forementioned stresses are hypothesized to induce the production of hypoxia-inducible factor 1a, vascular endothelial growth factors, and matrix metalloproteinase-9 through a cascade of reactions that ultimately leads to atrial fibrosis.14,20–22. The gene discussed is MMP9; the disease is atrial fibrillation.