In the pancreas, dysregulated GDH increases glutamate deamination reactions, induces an overreaction of insulin to amino acid consumption, promotes ATP formation, and stimulates insulin secretion [5]; in the kidneys, hyper glutamate catabolism leads to an increase in ammonia production [6]; and in the CNS, GDH abnormalities result in a disruption of the homeostatic balance of glutamate and its derivative γ-aminobutyric acid as inter-regulatory neurotransmitters, inducing epilepsy and related conditions [7]. This evidence concerns the gene GLUD1 and epilepsy.