Based on the above data, we propose the hypotheses that in chronic hyperammonemia increased activation of glycine receptors may contribute to neuroinflammation, including activation of microglia and astrocytes, and to increased membrane expression of TNFR1 and activation of the associated signal transduction pathway, leading to increased levels of extracellular glutamate and GABA. The gene discussed is TNFRSF1A; the disease is Hyperammonemia.