In this study, the authors demonstrated reduced Na+ current and Nav1.5/N-Cadherin clusters at junctional sites in the patient-derived hiPSC-CMs, suggesting that Nav1.5 may be part of a functional complex with adhesion molecules such as N-Cadherin, which reveals a non-canonical mechanism by which SCN5A mutations lead to ARVC cardiomyopathy [147]. The gene discussed is CDH2; the disease is arrhythmogenic right ventricular cardiomyopathy.