Central to this paradigm shift are cytotoxic CD8+ T cells, which mediate durable tumor control through antigen‐specific recognition and destruction of malignant cells.[1] Despite remarkable clinical successes, the majority of patients with solid tumors fail to achieve long‐term benefit from current immunotherapies, including immune checkpoint blockades (ICBs).[2, 3] A major impediment to durable responses is the profound immunosuppressive tumor microenvironment (TME), marked by hypoxia, nutrient deprivation, and elevated oxidative stress. The gene discussed is CD8A; the disease is neoplasm.