CD4+CD25+Foxp3+ Tregs have a strong potential to hinder the accumulation and effector function of tumor‐infiltrating CD8+ T cells through a variety of mechanisms.[28] On the other hand, TAMs could recruit CD4+CD25+Foxp3+ Tregs into the TME by releasing multiple chemokines, including CCL20, CCL22, to facilitate the establishment of tumor immunosuppressive micro‐environment.[11, 29] Therefore, we supposed that TAMs might induce the suppressed accumulation and function of CD8+ T cells through recruiting CD4+CD25+Foxp3+ Tregs into the TME of HCC patients with high Gal1 expression. The gene discussed is FOXP3; the disease is neoplasm.