In mdx mice, a genetic DMD model expressing non-functional dystrophin (further referred to as Dmd-mdx), Gonzalez et al. demonstrated that arrhythmias induced by β-adrenergic stimulation with isoproterenol, as well as the ensuing animal mortality, were significantly decreased after HC inhibition with Gap26 or Gap19 (115). This evidence concerns the gene DMD and cardiac arrhythmia.