Thus, it is not surprising that “hot” tumors—those with a higher density of tumor-infiltrating cytotoxic CD8 T cells—respond better to immune checkpoint blockade (ICB) and correlate with better clinical outcomes as compared with “cold” tumors, which show low or no immune cell infiltration in the TME (2, 3, 6, 7). The gene discussed is CD8A; the disease is neoplasm.