The concomitant Cx43—Nav1.5 interaction and their translational relevance was previously shown in a study which lead to a significant loss of Nav1.5 and severe ventricular arrhythmia [18] after deletion of the last five amino acids of Cx43 – representing a binding motif for tight-junction-protein-1. The gene discussed is GJA1; the disease is Ventricular arrhythmia.