Another mutation of FGF12, p.Q7R, reduced FGF12 expression and Na+ channel density and availability, leading to the development of BrS.12, 13 In contrast, abnormal mutations of genes encoding the Na+ channel, such as p.H1849R in SCN5A, can block the interaction and regulation of FGF12 and cause human arrhythmia.14 These studies suggested that the interaction of FGF12 and Na+ channels may play an important role in causing arrhythmia. Here, SCN5A is linked to cardiac arrhythmia.