Another mechanism in the tumor environment leading to exhausted T cells is the increased production of adenosine via sequential hydrolysis of adenosine-triphosphate (ATP) by the ectonucleoside triphosphate diphosphohydrolase-1 (CD39) and the ecto-5’-nucleotidase (CD73) [23,24,25]. This evidence concerns the gene ENTPD1 and neoplasm.