We have previously shown that enhanced GABAergic neurotransmission in cerebellum is responsible for motor incoordination in hyperammonemia and hepatic encephalopathy [6–8, 10, 27, 28] and that increased GABAergic neurotransmission is a consequence of neuroinflammation, especially of increased TNFα levels and increased activation of its receptor TNFR1 [10, 25]. Here, TNF is linked to Hyperammonemia.