Fatal ventricular tachyarrhythmias (FVTs) are a major cause of sudden cardiac death globally. Despite their clinical importance, current antiarrhythmic therapies remain constrained by limited efficacy and proarrhythmic risks. Although endogenous cardiac cholinergic signalling contributes to electrophysiological regulation, the therapeutic potential of targeting ventricular α4β2 nicotinic acetylcholine receptors (nAChRs), a pivotal component of this system, for FVT treatment remains to be elucidated.