ADO and neoplasm: These include respiratory hyperoxia, mild HT improving the oxygenation status of the tumor, antagonizing or downregulation of ADO receptors, inhibition of CD39 and CD73, co-blockade of immune checkpoint inhibitors CTLA-4 and PD-1/PDL-1, inhibition of the ENT-1 transporter or blockade of the ATP-release channel, HIF-pathway inhibition, enhancement of ADO degradation to inosine, and facilitation of AMP synthesis from ADO.