We cultured activated CD8+ T cells in conditional medium in vitro and found that PG indirectly regulates VEGF-A–VEGFR-2 by reducing the release of the inhibitory factor VEGF-A from the tumor cells to immunomodulate the expression of PD-1 on the surface of CD8 T+ cells, rather than directly acting on CD8+ T cells, and experimental verifications reveal that the downregulation of VEGF-A is due to the fact that PG reduces the phosphorylation of STAT3 in tumor cells, which additionally affects apoptosis, proliferation, and cycle biological processes mediated by STAT3 downstream (Yu et al., 2007). The gene discussed is KDR; the disease is neoplasm.