Thus, as already shown for other excitability disorders such as LQTS, BrS, or familial epilepsy (Crotti et al, 2005; Poelzing et al, 2006; Klassen et al, 2011), phenotypic variation in cardiac arrhythmia may be originated in the functional interaction of mutations in known predisposing genes (SCN5A) with additional mutations in novel genes as shown here with KCNK17. This evidence concerns the gene KCNK17 and familial long QT syndrome.