Brugada syndrome (BrS), characterized by the presence of coved-type ST-segment elevation followed by T-wave inversion in the right precordial electrocardiogram (ECG) leads in patients who have no structural heart disease but have a high risk of sudden cardiac death from ventricular fibrillation (VF), has captivated arrhythmia scholars and electrophysiologists for more than 2 decades. As a result, major progresses have been made toward a better understanding of the syndrome with respect to its genetic basis, underlying pathophysiology, and risk stratification.