Mutations in the cardiac isoform of the ryanodine receptor (RyR2) are the common genetic basis for CPVT (Lanner et al., 2010; Liu et al., 2017; Priori et al., 2001; Van Petegem, 2012; Zhao et al., 2015); however, recent genetic studies have identified novel calmodulin (CaM) mutations associated with the disease (Chazin and Johnson, 2020; Gomez-Hurtado et al., 2016; Jensen et al., 2018; Makita et al., 2014; Nyegaard et al., 2012; Wang et al., 2020). This evidence concerns the gene CALM3 and catecholaminergic polymorphic ventricular tachycardia.