Nevertheless, we explored a potential crosstalk between oncogenic signaling and stress response signaling in orchestrating immune TME of HCC and suggest a novel mechanism of HSF1-induced PD-L1 expression; moreover, based on the finding that HSF1 induced PD-L1 by regulating STAT3 signaling in HCC, a combination of HSF1 inhibitor or STAT3 inhibitor and PD-1 antibodies would be expected as more effective therapeutic approaches to target against TME in HCC, even pan-cancer. This evidence concerns the gene HSF1 and cancer.