Functionally CD39 can act in concert with CD73 to promote immunosuppression by converting ATP to immunosuppressive adenosine.17 Adenosine contributes to immunosuppression within the TME68 and the CD39 antagonist ARL-67156 enhances the function of intratumoral T cells.69 Deletion of the A2A adenosine receptor increases the efficiency of anti-tumor CAR T cells.70 Mixed bone marrow chimera experiments show that CD73 expression in CAFs limits T cell response and prevents tumor rejection.8 Consequently there is increasing interest in targeting these ectoenzymes as inhibitory checkpoints in cancer. This evidence concerns the gene NT5E and neoplasm.