We speculate that the incomplete oxidation of short-chain fatty acids due to SCAD deficiency may have produced a small mitochondrial oxidative deficiency, consistent with a previous report of 20% lower acetyl-CoA levels in the brain of Acads−/− compared with Acads+/+ mice [27]. The gene discussed is ACADS; the disease is hyperinsulinemic hypoglycemia, familial, 4.