Taken together with the present investigations that confirmed a lack of effect of these concentrations of flecainide and QX‐FL on the physiologically relevant luminal‐to‐cytoplasmic ion flux through RyR2 channels and, in the case of QX‐FL, any inhibition of a potential charge‐compensating cytosolic‐to‐luminal K+ flux (Figures 4, 5, 6), these data support the conclusion that the only mode of action underpinning flecainide's efficacy in CPVT patients is the inhibition of INa (Liu et al., 2011; Sikkel et al., 2013a; Bannister et al., 2015). The gene discussed is RYR2; the disease is catecholaminergic polymorphic ventricular tachycardia.