CAMK2G and familial dilated cardiomyopathy: Protein glycosylation (Clark et al., 2003) and oxidized CaMKII are significantly up-regulated in the DCM (Jay et al., 2006), therefore CaMKII activation and RyR2 phosphorylation has been proposed as a potential mechanism of heart failure, ventricular arrhythmias and apoptosis in this disease (Daniels et al., 2015).