ACOT1 and cardiomyopathy: Since enhanced FAs β-oxidation, following the oversupply of long-chain acyl-CoAs in diabetic hearts [41], [42] is attributable to initiation of oxidative stress and finally cardiomyopathy, the hydrolyzation of long-chain acyl-CoAs by ACOT1 is predicted to be an effective inhibition of increased FAs oxidation.