In conclusion, our study showed that CaMKII activation led to hyperphosphorylation of RyR2 (Ser2814) and RyR2 (Ser2808) during cardiomyocyte ischemia, which resulted in dissociation of the FKBP12.6-RyR2 complex, and increased intracellular Ca2+ content, which may contribute to the development of ventricular arrhythmias. This evidence concerns the gene CAMK2G and Ventricular arrhythmia.