However, it is not only cancer cells that release eADO to maintain specific immunoinhibitory phenotype [26]; indeed, dying T regulatory (Treg) cells within the TME provide both ATP molecules and CD39/CD73 ectoenzymes to sustain the ADO-rich TME, which in turn triggers immunosuppression in adjacent effector cells via A2AR [27]. The gene discussed is NT5E; the disease is cancer.