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). The gene discussed is DMD; the disease is Arrhythmia.