Either produced by tumor cells and/or by immune suppressive cells, ADO accumulates in tumor tissues where it suppresses T effector cell functions, reducing their proliferation, cytotoxic activity, and pro-inflammatory cytokine secretion, including IFN-γ, tumor necrosis factor (TNF)-β, and IL-2, by binding to purinergic receptors A2aR and, partially, A2bR [101,107,108,109,110,111,112]. This evidence concerns the gene ADO and neoplasm.