Considering the above, namely, that both the acute and chronic use of VPA can inhibit oxidative phosphorylation in cerebral mitochondria [15,35], it can be assumed that the VPA-induced activation of GDH and ALT is a compensatory mechanism aimed at restoring the energy metabolism, but this metabolic adaptation ensuring the availability of TCA cycle intermediates also leads to an increased production of ammonia, which, with reduced GS activity in the brain and a normally functioning liver, can be the culprit of encephalopathy. This evidence concerns the gene GLUL and Encephalopathy.