Injury of the gut epithelium, e.g. induced by DSS, not only increases colonic eATP levels37 but also upregulates NTPDases such as CD39.42 During the course of mucosal inflammation, increasing expression of NTPDases leads to ATP breakdown and release of extracellular adenosine, which has been implicated as an endogenous protective reagent in IBD.43 A2A and A2B receptors were suggested to contribute to the anti‐inflammatory action of adenosine.44, 45, 46 We found here that ILC3s express high levels of A2A receptor, and activation of the A2A receptor promotes IL‐22 production from ILC3s. This evidence concerns the gene IL22 and inflammatory bowel disease.