Our previous studies indicate that an early, long-term, cardiomyocyte-restricted- (CR-) PPARβ/δ deletion in mice impairs myocardial FAO and bioenergetics, leading to cardiac dysfunction, progressive myocardial lipid accumulation, cardiac hypertrophy, and congestive heart failure [12, 14]. The gene discussed is PPARD; the disease is cardiac hypertrophy.