CXCR5 and neoplasm: One possible explanation is that the dominant clones in ICI treatment are the newly emerged distinct clones, rather than the reinvigoration of pre‐existing ones.[37] Several reasons may account for this phenomenon (i) exhausted T cells having difficulty reinvigorating antitumor immunity due to their epigenetic stability,[38, 39] (ii) CXCR5+CD8+ T cells proliferating only in lymphoid tissues,[40] and (iii) the local activation of tumor‐infiltrating lymphocytes (TILs) being insufficient to induce antitumor responses.[41]