These results indicate that753b is promising as a potential therapeutic option for NAFLD andNASH-related HCCs.136 Furthermore, NASHhas shown that it limits antitumor surveillance of HCC treated withimmunotherapy by promoting the exhaustion of CD8+ PD1+ T cells inthe liver, suggesting a potential therapeutic strategy to improvethe immune therapy response in this environment.137 NASH-related HCC has a unique immune microenvironment thatinfluences its pathogenesis and response to therapy.138. This evidence concerns the gene CD8A and hepatocellular carcinoma.