In support, in the current study, we observed strong negative correlations between serum LPS and intrahepatic Tlr4 and Myd88, thereby in concordance with the observation that initial unrestricted proinflammatory responses to bacterial products contribute to ‘LPS immunotolerance’ and the immunosuppressed intrahepatic phenotype observed in advanced cirrhosis and HCC. This evidence concerns the gene MYD88 and hepatocellular carcinoma.