Based on CPVT mouse-model experiments which showed that Ca2+/calmodulin-dependent serine-threonine protein kinase II (CaMKII) was related to arrhythmic events evoked by β-adrenergic stimulation, Pasquale et al. demonstrated that KN-93, an antiarrhythmic CaMKII inhibitor, also attenuated putative DADs and abnormal multifocal Ca2+ transients [105]. This evidence concerns the gene CAMK2G and catecholaminergic polymorphic ventricular tachycardia.