Therefore, increased expression of CXCR5 on both suppressive subsets in patients with CLL could support entry into TME of functional Treg subsets, promoting tumor immune evasion by suppressing antitumor T-cell responses not only through a contact-dependent (cytotoxic T-lymphocyte-associated protein 4/CTLA-4 expression in aTreg cells) but also cytokine-dependent mechanism [43,44]. The gene discussed is CXCR5; the disease is B-cell chronic lymphocytic leukemia.