Compared with nontumour areas, the TME of HCC has significantly more CD4 + CD25 + FoxP3 + Treg cells and significantly fewer CD8 + T cells; and CCL2 and CCL5 produced by tumour cells play an important role in regulating this phenotype At this high level, Treg cells can impair the effector function of CD8 + T cells, significantly reducing the expression of granzyme A, granzyme B, and perforin in infiltrating CD8 + T cells, and promoting disease progression in HCC patients [93, 94]. The gene discussed is CD8A; the disease is neoplasm.