The immunosuppressive tumor microenvironment in HBV-HCC is particularly amenable to PD-1 inhibitor-mediated reversal, as supported by evidence that ICIs reduce HBV DNA levels in HBV-HCC patients without HBV reactivation (31), and basic studies specific to tislelizumab (the ICI used in our case) demonstrate its ability to induce high PD-L1 expression in HBV-infected tissue microenvironments and alleviate immunosuppression more efficiently via its high affinity for PD-1 (32). This evidence concerns the gene CD274 and neoplasm.