Until recently, the drug's effectiveness against CPVT (e.g. [7–10]) has been considered to be a direct consequence of inhibition of RyR2 ryanodine receptors (e.g. [7,60]), which in intact cardiomyocytes would require cell entry of the drug to access RyR2s in the sarcoplasmic reticulum membrane. Here, RYR2 is linked to catecholaminergic polymorphic ventricular tachycardia.