CaMKII inhibition by KN-93 was also shown to reduce the incidence of stress-induced ventricular tachycardia in a junction knock-out mouse model which presents with a phenotype similar to CPVT (RyR2 channels display CaMKII-dependent hyperphosphorylation). The gene discussed is CAMK2G; the disease is catecholaminergic polymorphic ventricular tachycardia.