The significant role of CaMKII in arrhythmogenesis is supported by the fact that overexpressed CaMKII increases the incidence of VF/VT [94], whereas the decrease in phosphorylated CaMKII levels induced by SERCA2a gene therapy prevented the frequency-dependent decrease in conduction velocity and was associated with arrhythmia suppression in MI pigs [93]. This evidence concerns the gene CAMK2G and ventricular fibrillation.