Viral delivery of CASQ2 infected ~50% of myocytes, restored CASQ2, triadin (TrD), and junction (JnC) levels to ~80–90% of wild-type levels. This led to reversal of jSR structural abnormalities, including jSR width normalization (from 37 ± 1.2 nm in KO to 21 ± 0.3 nm in treated; p < 0.001), reduced triggered activity during β-adrenergic stimulation (from 70% to 5% of myocytes; p < 0.001), and suppression of in vivo ventricular tachycardia (from 15/15 to 1/10 mice after epinephrine; p < 0.001). No histological toxicity observed. Demonstrated durable structural and functional rescue. This evidence concerns the gene CASQ2 and ventricular tachycardia.