A2BR blockade promotes DC activation (e.g., increased CD86 expression on CD11b- DCs), increases CD4+ and CD8+ T cell IFN-γ production, and tumor cell IFN-γ and CXCL10 expression (86), which supports the therapeutic potential of A2BR antagonists in enhancing antitumor immunity. This evidence concerns the gene CXCL10 and neoplasm.