Immunotherapy has shown promising in advanced hepatocellular carcinoma (HCC), yet the limited response rate to PD-1 blockade underscores the need to understand resistance mechanisms. Our study uncovers a novel resistance mechanism in which immunotherapy-induced IFNG signaling promotes tumor-derived IL18BP secretion via the STAT1/IRF1 axis. IL18BP functions as a secreted immune checkpoint that competitively inhibits IL18 signaling, thereby impairing IL18-mediated CD8+ T cell activation and metabolic reprogramming, ultimately driving immune evasion and immunotherapy resistance in HCC.