As inhibition of OAT transamination activity in acute hyperammonemia leads to normalization of glutamate and glutamine levels consecutively restoring 2-oxoglutarate concentrations, it is a valuable therapeutic strategy to simultaneously tackle impaired glutamatergic neurotransmission, glutamine-mediated brain edema and cerebral energy depletion, which are the central culprits of hyperammonemia-induced neurotoxicity. This evidence concerns the gene OAT and Hyperammonemia.