To investigate the mechanism by which Tα1 promotes the differential recruitment of T-cell subsets, we measured the levels of chemokines in the melanoma tumor microenvironment and found increased levels of Cxcl9 and Cxcl10, known to promote tumor lymphocyte infiltration, and decreased levels of Ccl22, implicated in intratumoral recruitment of Treg, upon treatment with anti–CTLA-4 antibody and Tα1 (Fig 6A). The gene discussed is CXCL9; the disease is melanoma.