Thus, targeting CD73 could prove beneficial under several respects, directly targeting NAD+ biosynthesis in the malignant epithelial cells (as those used in our study), but also preventing CD73 activity on the stromal cells that are present within the tumor, which might contribute to the generation of NR and adenosine in the tumor extracellular microenvironment and thereby promote tumor growth [61]. The gene discussed is NT5E; the disease is neoplasm.