Expression of PD‐1 on activated T cells occurs later in their effector phase compared to CTLA‐4, meaning PD‐1 inhibitory regulation occurs later in the immune response.2, 25 Engagement of PD‐1 by either of its ligands, PD‐L1 or PD‐L2 expressed on tumor cells, DCs or NK cells, suppresses T‐cell activity by abrogating TCR signalling, prompting an exhaustive phenotype.33 Given its delayed role, PD‐1 is thought to be more significant within the TME and therefore an important mechanism of tumor‐immune resistance. The gene discussed is CD274; the disease is neoplasm.