Our results suggest a promising future avenue of drug development, namely exploitation of nontraditional ion channel drug targets, which allows for precision-targeted and mutation-specific pharmacotherapy for both LQT3 mutations and an enhanced mexiletine for ventricular tachycardia, with a more favorable side effect profile.PerspectivesCOMPETENCY IN MEDICAL KNOWLEDGE: Class I antiarrhythmic therapies remain suboptimal given the inability to predict efficacy and potential proarrhythmic side effects. This evidence concerns the gene SCN5A and ventricular tachycardia.