Three recent publications have utilized preclinical mouse models to evaluate the role of adenosine signaling in pancreatic cancer and have collectively shown genetic deletion of CD73 or treatment with CD73 small molecule inhibitors in syngeneic or genetic mouse models significantly reduces the development and progression of pancreatic cancer and promotes increased anti-tumor immunity; however, there are some differences in the models and findings which we want to highlight (4–6). This evidence concerns the gene NT5E and neoplasm.