However, these immunostimulatory effects are counterbalanced by immunosuppression via several mechanisms, mainly upregulation of PD-L1 levels on tumor cells via INF-γ released by CD8+ T cells and of PD-1 levels on CD8+ tumor infiltrating lymphocytes (TILs), contributing to T-cell exhaustion (14, 15). The gene discussed is CD8A; the disease is neoplasm.