Beyond diLQTS and cLQTS, INa-L in cardiomyocytes can be increased by acquired conditions such as heart failure.[42] Whether variants in SNTA1 increase the risk of arrhythmias in heart failure patients has not been tested, but would fit with a previous study showing that the S1103Y polymorphism in SCN5A confers an increased risk of arrhythmogenesis in patients with heart failure.[43] In summary, our study demonstrated that a novel SNTA1 variant, p.E409Q, increased the INa-L and is a potential mechanism for acquired lethal ventricular arrhythmias. This evidence concerns the gene SCN5A and cardiac arrhythmia.