Studies have shown that IFN-α improved glucose metabolism in the TME by inhibiting HIF-1α signaling, decreasing glucose consumption, activating mTOR-FOXM1 signaling, promoting the toxic effects of CD8+T cells, and enhancing PL-D-blocked immune responses to achieve anti-HCC (Hu et al., 2022). This evidence concerns the gene MTOR and hepatocellular carcinoma.