Collectively, these results suggest that the genetic inhibition of mPTP in the CPVT model led to higher ROS production, activation of the CaMKII pathway, and subsequent hyperphosphorylation of RyR2 in the DKO model, thus, further exacerbating RyR2 dysfunction. The gene discussed is CAMK2G; the disease is catecholaminergic polymorphic ventricular tachycardia.