In the development of liver failure, the altered hepatic inflammatory status and systematic immune dysfunction, featured by apparent infiltration of multiple inflammatory cells (e.g., neutrophils and macrophages) in the liver and an abrupt increase of serum pro-inflammatory cytokines (e.g., TNF-α and IL-6), ultimately contribute to liver necrosis and liver failure34–37. This evidence concerns the gene IL6 and Hepatic failure.