The results showed that Texterm cells might trigger the recruitment of regulatory T cells (Tregs) into the TME via CCL5‐CCR4 binding, thus promoting immune suppression, which is consistent with the literature.[22] Additionally, Texterm cells might facilitate tumor cell immune evasion through the TIGIT–PRR3 signaling axis (Figure 3H). The gene discussed is CCL5; the disease is neoplasm.