Divergence of the net metabolic flux of fatty acids from the oxidative pathway leads to myocardial triglyceride accumulation and development of lipotoxic heart disease in mouse models that overexpress either PPARα or long-chain acyl-CoA synthetase (ACSL) [20], [21], or are long-chain acyl-CoA dehydrogenase-deficient (LCAD) [22]. Here, SLC27A1 is linked to heart disorder.