A compelling application of base editing was demonstrated in a model of catecholaminergic polymorphic ventricular tachycardia (CPVT), where correction of a splice-site mutation in RYR2 successfully abolished arrhythmogenic calcium transients in iPSC-CMs, underscoring the therapeutic promise of these refined editing platforms [143]. This evidence concerns the gene RYR2 and catecholaminergic polymorphic ventricular tachycardia.