Experiments with cardiac-specific deletion of ACC2 (acetyl-CoA carboxylase 2), a vital enzyme, catalysing the carboxylation of acetyl-CoA to malonyl-CoA, which could inhibit carnitine-palmitoyl-CoA transferase I, the rate-limiting step in FA uptake and oxidation by mitochondria, suggested that enhanced cardiac FAO does not cause cardiomyopathy in non-obese mice. This evidence concerns the gene ACACB and cardiomyopathy.