We recently showed (10) that long-term treatment with therapeutic doses/concentrations of empagliflozin (EMPA), an inhibitor of sodium/glucose cotransporter 2 (SGLT2) in clinical use to treat type II diabetes and nondiabetic heart failure (11–13), completely rescues abnormally reduced peak INa in ventricular cardiomyocytes from the most commonly used animal model for DMD, the dystrophin-deficient mdx mouse (14). The gene discussed is SLC5A2; the disease is type 2 diabetes mellitus.