Similarly, Triadin mutations are thought to result in reduced protein levels, which in turnincreased calcium currents and prolonged cardiac action potentials, and increased spontaneous calcium release events caused by cellular and SR calcium overload, which is the basis of TRDN mutation leading to CPVT and LQTS (69, 123). Here, TRDN is linked to catecholaminergic polymorphic ventricular tachycardia.