Whilst ATP promoted kidney IRI predominantly via the P2X7 receptor [22], an effect which can be abrogated by administration of a P2X7 receptor antagonist up to 6 h post reperfusion [32], CD39-adenosine protection is mediated via A1, A2A and A2B receptors depending on the predominant cell type involved [reviewed in 33]. The gene discussed is P2RX7; the disease is medical procedure.