KCNA3 and familial long QT syndrome: Reviewed extensively elsewhere [4], ventricular repolarization is largely modulated by potassium outward channels where perturbance from acquired conditions such as structural disorders (myocardial ischemia, bundle branch block, antiarrhythmics, electrolyte disturbances) or congenital disorders with loss- or gain-of-function mutations affecting the potassium channels can result in QT prolongation (congenital long QT syndrome (LQTS)) or shortening (short QT syndrome, J wave syndromes), respectively, and ultimately pro-arrhythmias [7].