SLC6A8 and heart failure: Wallis et al. (36) nicely demonstrated that the overexpression of CT1 in transgenic mice induces an excessive accumulation of creatine inside the myocytes, with an abnormally high intracellular creatine pool (66 ± 6 nmol/mg protein in wild-type controls vs. 133 ± 52 nmol/mg protein in CT1-overexpressing transgenic mice), accompanied by left ventricular dysfunction, myocardial hypertrophy, and heart failure.