Ventricular tachycardia arising from a healed myocardial infarction scar continues to be a significant cause of morbidity and mortality. Drug therapy has been inadequate to meet this challenge, and implantable devices are limited by expense and technical problems. We have proposed the use of gene therapy for cardiac arrhythmias. In this review, we present a model of postinfarct ventricular tachycardia, a method for gene delivery to this area, and results of KCNH2-G628S gene transfer to manipulate cellular refractory properties in the arrhythmia model.