The possible mechanism of anti-PD-1 therapy in HBV-related HCC could be explained by the overexpression of PD-1 to inhibit and deplete CD8+ resident memory T cells (TRM cells) [41, 42], which have been proved to be enriched in HBV infected liver, and cause a partial immune response [42, 43]. Here, CD8A is linked to hepatocellular carcinoma.