The additional CAAs released by initial dying tumor cells trigger a new round of the sequence and amplify the magnitude of the immune response with each subsequent round.[1] However, if tumors persist, CD8+ T cells become exhausted, characterized by an orderly loss of effector functions, impaired proliferation, and the upregulation of inhibitory receptors (e.g., PD‐1, Lag‐3, Tim‐3;[2, 3]). This evidence concerns the gene CD8A and neoplasm.