In LQT3, SCN5A mutations typically lead to an increase in late sodium current (INaL), a small inward current that persists throughout the duration of the AP plateau and repolarization phase leading to AP prolongation that can in turn predispose to torsades de pointes ventricular arrhythmias and sudden cardiac death (SCD) [4,5]. The gene discussed is SCN5A; the disease is long QT syndrome 3.