CD8A and neoplasm: A traditional theory represents the major mechanism by which PD-1/PD-L1 ICB reactivates exhausted CD8+ T cells (TEX) in tumor microenvironment (TME), thereby restoring the autologous antitumor immunity.2 However, this theory cannot explain why only a portion of TEX can response to PD-1/PD-L1 ICB and even “cold” tumors responses to ICB.