Treatment of HTLV-1 specific CD8+ cells with anti-PD-L1 antibody increased the production of IFN-γ, TNF-α, and expression of CD107 suggestive of reactivation of exhausted T cells.13 These results suggest that increased expression of PD-1/PD-L1 checkpoint might contribute to chronic HTLV-1 infection, immune evasion and ultimately development of ATLL representing a potential therapeutic target to enhance immune response against viral infections.14 This evidence concerns the gene CD8A and viral infectious disease.