Worsening fibrosis undoubtedly plays a role in the progression of conduction defects with age in the Scn5a+/− mouse model; however, this mouse also demonstrates increased susceptibility to ventricular arrhythmias from a young age (8–36 weeks), when fibrosis would not be expected to play an appreciable role.7 This evidence concerns the gene SCN5A and Ventricular arrhythmia.