CD274 and neoplasm: For instance, programmed death ligand‐1 (PD‐L1) binds to programmed death‐1 (PD‐1) on T cells, triggering T cell deactivation and enabling tumor cells to evade the host's immune response.[3] GC‐derived exosomes boosted the accumulation of PD1+ TAM (tumor‐associated macrophage), which further compromised CD8+ T cells' effectiveness and obstructed GC advancement.[4] Additionally, accumulating evidence indicates that the tumor microenvironment (TME) is not only pivotal in tumorigenesis but also intimately associated with the efficacy of immunotherapy.[5] Derks et al.