Interestingly, tumor-derived CD73-dependent adenosine promoted growth, neovascularization, and metastasis of subcutaneous B16F10 melanoma tumors and this was linked to infiltration and polarization of macrophages: genetic or pharmacologic inhibition of CD73 on the B16F10 melanoma cells significantly reduced the number of tumor-infiltrating macrophages recruited to subcutaneous B16F10 melanoma tumors on CD73−/− mice when compared to untreated B16F10 wildtype tumors on CD73−/− mice. This evidence concerns the gene NT5E and neoplasm.