Our study suggested that an I/R-injured myocardium was more susceptible to VT with a higher expression of ox-CaMKII, p-CaMKII, and p-RyR2 (Ser2814) while upregulation of miR-145 dramatically decreased the activation of CaMKII and RyR2 (Ser2814) thus reducing the risk of arrhythmia. The gene discussed is CAMK2G; the disease is cardiac arrhythmia.