Because of the association between C-terminus RYR2 variants and an increased risk for ventricular arrhythmia,6 structural change near the C-terminus may explain the ease of inducibility and intractability in our patient’s case; histidine insertion in the RYR2 protein may induce increased release of store-overload-induced Ca2+ and/or a markedly reduced threshold for the occurrence of Ca2+ release.5 However, the exact mechanism is unknown because cases of CPVT involving histidine insertion in the RYR2 protein have not been reported previously. The gene discussed is RYR2; the disease is catecholaminergic polymorphic ventricular tachycardia.