Extracellular adenosine has emerged as an important regulator of immunological processes within the tumor microenvironment and is thought to diminish the effectiveness of T-cell checkpoint inhibiting drugs as well as anti-tumor immunity in general.1–3 Adenosine triphosphate (ATP), released from necrotic or damaged cells, is hydrolyzed to adenosine by the sequential action of two ectonucleosidases working in tandem: CD39 (ENTPD1) and CD73 (NT5E). This evidence concerns the gene NT5E and neoplasm.