The dual effects of tislelizumab are primarily mediated through the following pathways: First, in reversing HBV-specific T-cell exhaustion: within the HBV-HCC tumor microenvironment, HBV-specific CD4+ T cells highly express exhaustion markers (e.g., PD-1, Tim-3), impairing their IFN-γ secretion; tislelizumab binds PD-1 with high affinity (its Fc segment is engineered to avoid T-cell phagocytosis (25) to block the PD-1/PD-L1 pathway, restoring the cytotoxic activity of HBV-infected hepatocytes (28). This evidence concerns the gene HAVCR2 and hepatocellular carcinoma.