Given that both Th1 and Th17 autoreactive T cells are pathogenic for autoimmune diseases [52–54], continue efforts to identify mechanisms by which adenosine enhances or inhibits should allow us to manage undesired effects of AR agonists on the Th17 autoimmune response and improve the therapeutic goal of controlling both Th1 and Th17 responses in autoimmune diseases. The gene discussed is AR; the disease is autoimmune disease.