More recently, Schweitzer et al. (2017) suggested that pharmacological enhancement of [Ca2+]m suppressed arrhythmia in a model of catecholaminergic polymorphic ventricular tachycardia (CPVT), a condition characterized by mutations in the RyR macromolecular complex that renders channels hyperactive. This evidence concerns the gene RYR2 and catecholaminergic polymorphic ventricular tachycardia.