Overexpression of CD73 enhances ADO production in tumor cells, immunosuppressive cells (e.g., Tregs, MDSCs), and tumor endothelial cells.[57] Under tumor hypoxia, CD73 expression is upregulated, leading to excessive ADO accumulation, which promotes immune escape by activating the A2A and A2B ADO receptors in the TME. This evidence concerns the gene NT5E and neoplasm.