In our previous works, we have found similar changes (fragmentation of CRUs), i.e., reduction in size of RYR2 clusters, in mouse models lacking calsequestrin-2 (CASQ2) and carrying human mutations in CASQ2 linked to catecholaminergic polymorphic ventricular tachycardia [47,48,49]. This evidence concerns the gene RYR2 and catecholaminergic polymorphic ventricular tachycardia.