Specifically, HBV-DNA-Pol regulates PD-L1 transcription by repressing PARP1 nuclear translocation, which results in excessive PD-L1 expression in malignant hepatocytes, leading to PD-L1/PD-1 axis-mediated tumor immune evasion, and ultimately, HCC development (Fig. 7). Here, PARP1 is linked to neoplasm.