Consistently, a recent study showed that increasing mitochondrial FAO by genetic deletion of acetyl-CoA carboxylase 2 that enhanced FAO by relieving the inhibition of CPT-1 was sufficient to prevent the development of obesity induced cardiomyopathy, in part via the inhibition of mitochondrial dysfunction [38]. The gene discussed is ACACB; the disease is obesity due to melanocortin 4 receptor deficiency.