The p.Q7R mutation reduced binding to the NaV1.5 C‐terminus and Na+ channel current density, leading to Na+ channel loss‐of‐function phenotype consistent with that in BrS.12, 13 Furthermore, Musa et al reported that a variation in SCN5A (p.H1849R) blocks the regulation of FGF12 and causes human arrhythmia.14 This evidence highlighted that the variations in FGF12 may affect the interaction between FGF12 and Na+ channel, leading to arrhythmia. Here, SCN5A is linked to cardiac arrhythmia.