In summary, the present study suggest that following acute liver failure, CCL2 induced microglia activation and subsequent inflammatory cytokines release play an important role in neurological dysfunction during HE, and inhibition of CCL2 action using CCL2 receptor inhibitors, CCL2 neutralizing antibody or knockdown of CCL2 expression may be a potential therapeutic method for patients suffering from HE. The gene discussed is CCL2; the disease is acute liver failure.