Taken together, these results indicated that TNKS1BP1 knockdown could increase the expression level of PD-L1 in tumor cells by activating the JAK2/STAT3 signaling pathway, as well as the infiltration and cytotoxicity of CD8+ T cells, which jointly contributed to the increased sensitivity to anti-PD-L1 immunotherapy in HCC patients. The gene discussed is JAK2; the disease is neoplasm.