2′3′‐cGAMP seemed to have effectively circumvented this limitation by promoting CD8+ T‐cell terminal differentiation via the activation of tumor‐infiltrating DC, given that the combination therapy recruited CD8+ T‐cells whose expression is not only low in PD1 but also high in KLGR1, a terminal differentiation marker for effector CD8+ T‐cells [40]. The gene discussed is CD8A; the disease is neoplasm.