We found that CSCs, highly expressed immune checkpoint molecules such as NECTIN2/3 and LGALS9, interacted with suppressive CXCL13+ T cells through the ligand‐receptor pairs: TIGIT‐NECTIN2/3 and LGALS9‐HAVCR2, which contribute to the increase of Tregs and inhibition of the activation and proliferation of cytotoxic T lymphocytes, thus providing an immunosuppressive niche that is critical to tumor cell immune escape. The gene discussed is CXCL13; the disease is neoplasm.