Tumor-intrinsic pathways in HCC also modulate immune escape: CTNNB1 mutations and WNT-β-catenin activation suppress CCL5 and DC recruitment, impair NKG2D ligand expression on HCC cells, and reduce NK-cell cytotoxicity [71]; p53 loss and CDK20 activation increase MDSC infiltration [72]; MYC overexpression, seen in 50–70% of cases, upregulates PD-L1 [73]; and chronic HBV infection elevates PD-L1 on Kupffer cells, leukocytes, and LSECs, enhancing immune suppression [12]. This evidence concerns the gene CCL5 and hepatocellular carcinoma.