To the Editor: In their review article, Eltzschig et al.(Dec. 13 issue) 1 discuss a number of new concepts regarding purinergic signaling in ischemia and reperfusion, acute lung injury, and inflammatory bowel disease. However, a drawback is the lack of any message about purinergic signaling in acute gouty arthritis, one of the most common inflammatory diseases. Acute gouty arthritis is known to be caused by a first signal to induce production of pro–interleukin-1β and a second signal to activate the NLRP3 inflammasome, which results in the production and secretion of interleukin-1β. 2 In October 2012, Riteau et al. reported that uric acid induces the active release of intracellular adenosine triphosphate (ATP) to the outside of human macrophages. 3 Moreover, they found that extracellular ATP may act through the P2X7 receptor to amplify ATP release and that both ATP and adenosine diphosphate act through an autocrine loop on other purinergic receptors, such as the P2X and P2Y receptors, leading to activation of the NLRP3 inflammasome. 3 These findings suggest that purinergic signaling is a critical mechanism in acute gouty arthritis. Therefore, purinergic signaling might be a new target for management of acute gouty arthritis.