Non-alcoholic fatty liver disease (NAFLD) is globally prevalent and can progress to NASH, significantly increasing the risk of HCC.601 Unlike viral hepatitis, which features organized inflammatory foci, inflammation induced by NAFLD/NASH typically involves scattered inflammatory infiltrates.582 Preclinical evidence suggests that NAFLD/NASH-related HCC is characterized by reduced CD4+ T cell activity within tumors, loss of tumor surveillance function by CD8+PD-1+T cells, and pro-tumorigenic functions of NKT cells and Th17 cells. This evidence concerns the gene CD8A and metabolic dysfunction-associated steatotic liver disease.