One such defect is epigenetic changes in the molecular machinery of autophagy, leading to poor efflux of ATP from dying tumor cells [21] and another defect being the overexpression of ectonucleoside triphosphate diphosphohydrolase 1 (ENTPD1, best known as CD39) or 5'-nucleotidase, ecto (NT5E, best known as CD73) which are membrane-bound nucleotidases that degrade extracellular ATP [22] to ADP, AMP, adenosine, and inorganic phosphate. This evidence concerns the gene ENTPD1 and neoplasm.