A recent study used mathematical modeling to demonstrate that human variants identified in the CaMKII phosphorylation motif of Nav1.5 confer arrhythmia susceptibility by mimicking the phosphorylated channel (Koval et al., 2012), while an earlier study examined the role of CaMKII regulation of SR Ca2+ release in increased incidence of afterdepolarizations in Timothy syndrome (Thiel et al., 2008). This evidence concerns the gene CAMK2G and Arrhythmia.