An in vitro electrophysiological analysis of the functional consequence of the p.L1785Q mutation has shown that it results in increased late persistent INa current, but also in a reduction of the total INa (Kanters et al., submitted), suggesting that the electrophysiological phenotype may be a combination of Brugada syndrome and LQTS, as previously described for SCN5A mutations [63], e.g. the p.E1784K mutation [64]. The gene discussed is SCN5A; the disease is familial long QT syndrome.