The Scn5a haploinsufficient mouse model (Scn5a+/−) has emerged as a powerful tool to study arrhythmia syndromes associated with loss-of-function Na-channel mutations,2 in particular Brugada syndrome (BrS), which is characterized by a risk of sudden cardiac death (SCD) due to ventricular fibrillation (VF) in patients with structurally normal hearts3 and poses a significant challenge for clinicians. Here, SCN5A is linked to ventricular fibrillation.