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"We showed that a loss-of-function mutation in FGF12 that eliminates Na + channel modulation is associated with Brugada syndrome, an inherited cardiac arrhythmia[ xref ], and a mutation in the cardiac Na + channel gene SCN5A that affects FGF12 interaction and Na V 1.5 channel function in ventricular myocytes leads to a life-threatening arrhythmia syndrome[ xref ]."

"Sodium channel fast inactivation is modulated by alpha subunit interaction with a family of cytoplasmic proteins termed fibroblast growth factor homologous factors (FHFs). In this paper, we report that all A-type FHFs exert rapid onset long-term inactivation on Nav1.6 and other sodium channels."