Therefore, our result provides believable proofs to support that SALL4 acts as a critical factor in HBV-maintained immune tolerance and HCC progression, and to elucidate the role of chronic virus infection in CD8+T cell exhaustion and tumor progression via pSTAT3-SALL4-miR-200c-PD-L1 axis, a mechanism of immune tolerance from intrinsic (e.g., HBV-induced PD-L1 expression on hepatocytes) to extrinsic (e.g., hepatocyte PD-L1-induced T cell exhaustion) pathways. The gene discussed is SALL4; the disease is neoplasm.