The heart is an electromechanical pump, and gap junction channels formed by connexin-43 (Cx43) ensure coupling between cardiac myocytes to enable the transmission of electrical and molecular signals, resulting in coordinated contractions [8,9], while the downregulation of Cx43 and/or channel dysfunction, as well as abnormal Cx43 topology, jeopardize synchronous cardiac electromechanical functions and render the heart prone to developing arrhythmias, including potentially lethal ventricular fibrillation (VF) [10,11]. Here, GJA1 is linked to ventricular fibrillation.