We have previously shown that exercise training reduces CaMKII oxidation, CaMKII‐dependent RyR2‐S2814 phosphorylation, arrhythmogenic Ca2+ release, and arrhythmias in the RyR2‐RS CPVT1 mouse model (Manotheepan et al., 2016). Here, CAMK2G is linked to catecholaminergic polymorphic ventricular tachycardia 1.