First, despite higher expression of cytotoxic effector molecules, granzymes and perforin, and potent cytotoxicity in vitro, CX3CR1+CD8+ T cells show lower expression of CXCR3 and L-selectin (CD62L; refs. 13–17), trafficking receptors needed for entry across the tumor microvasculature and lymphoid organ high endothelial venules, respectively (18–20), which allows the CX3CR1+ subset to remain in circulation after initial response while CX3CR1– subsets traffic to the TME and mediate antitumor efficacy (13, 15). The gene discussed is CD8A; the disease is neoplasm.