Cerebral ischemia leads to rapid elevation in extracellular adenosine concentrations due to the breakdown of extracellularly released ATP and the selective downregulation of concentrative nucleoside transporter 2 (CNT2); however, this adenosine elevation did not appear to depend on either CNT3 or equilibrative nucleoside transporter-1 (ENT-1), suggesting that this adaptive nucleoside transporter response contributes to the extracellular accumulation of adenosine during ischemia [11,12,13]. Here, SLC29A1 is linked to ischemia.