Autonomic imbalances in OSA are caused by negative thoracic pressure during periods of hypopnea, resulting in alternations in baroreceptor and chemoreceptor reflexes.39 These derangements can favor either profound vagal activity, leading to bradyarrhythmia, or sympathetic activation favoring tachyarrhythmias.40 This cascade deranges cardiomyocyte ion exchange through action on sodium channels, potassium channels, and gap junction proteins, generating inappropriate action potentials and triggering arrhythmia.41–43. The gene discussed is KCNA3; the disease is cardiac arrhythmia.