Transgenic mice with cardiac- restricted over-expression of PPARα (myosin heavy chain [MHC]-PPARα mice) exhibit a cardiac metabolic phenotype which is strikingly similar to that of the diabetic heart with increased FFA utilization and decreased uptake and oxidation of glucose, presenting features of lipotoxic cardiomyopathy without hyperlipidemia or hyperglycemia, including ventricular hypertrophy and dysfunction associated with myocardial lipid accumulation, which is exacerbated by a high fat (HF) diet enriched in long-chain FFA (LCFA) [3], [6], [10]. The gene discussed is PPARA; the disease is Ventricular hypertrophy.