The steps involved in HE include: firstly, liver injury causes hyperammonemia; secondly, hyperammonemia causes oxidative stress in both liver and brain; thirdly, the mitochondria located in the GAD2-expressing population in SNr are susceptible to oxidative stress attack, making SNr becomes the target of hyperammonemia; fourthly, mitochondrial dysfunction in SNrGAD2 population results in the hyperactivation of neuronal cells; fifthly, increased of GABAergic tone leads to hepatic encephalopathy. The gene discussed is GAD2; the disease is hereditary elliptocytosis.