The severe clinical consequences described in the most frequent inborn FAO disorders (MCAD, LCHAD, or very-long-chain acyl-coA dehydrogenase (VLCAD) deficiencies) warn us of their importance in postnatal life [23,24]; however, adequate FAO is also required earlier for fetal and placental energy support. This evidence concerns the gene ACADL and very long chain acyl-CoA dehydrogenase deficiency.