When this crosstalk is interrupted, a potent immune response toward ICIs was shown to occur in a murine model of HCC due to the inhibition of mTORC1-dependent PD-L1 production and the presence of PD-L1+ exosomes, suggesting that metabolic intervention by epigenetic regulation, such as targeting HMGB1, can also be a novel therapeutic target for ICI resistance [49,90]. Here, CD274 is linked to hepatocellular carcinoma.