We found in BrS-hiPSC-CMs: (i) The variants in SCN1B (c.629T > C/p.L210P and c.637C > A/p.P213T) led to a loss of function of sodium channels showing a significant reduction of APA and Vmax as well as sodium channel currents resulted from reduction of activation and enhancement of inactivation as well as decelerated recovery from inactivation of sodium channels; (ii) BrS-hiPSC-CMs displayed higher sensitivity responding to ajmaline and carbachol showing enhanced changes of action potential characteristics and increased arrhythmia events. This evidence concerns the gene SCN1B and Arrhythmia.