Hundreds of SCN5A variants have been reported leading to abnormal function of sodium ion channels and myocardial repolarization disorder [18, 19], including BrS, LQTS, SSS, etc. Abnormal sodium ion channels caused by SCN5A gene variant can be activated by high temperature, so BrS has a higher probability of incidence in high temperature regions which may help to explain the summer aggregation of SUD in some epidemic areas [20]. Here, SCN5A is linked to familial long QT syndrome.