These findings may partially explain the failure of anti-PD1 monotherapy in GC patients and further indicated that the key feature of CD8+ T cells in GC is the low frequency, not the defect of function by PD-1, meaning that increasing the recruitment of CD8+ T-cell infiltration in tumor lesions is likely more critical to boosting the antitumor immunity rather than antagonizing PD-1 alone for GC patients. This evidence concerns the gene CD8A and neoplasm.