In various states of IBD, ILC3s have been regarded as a double-edged sword that can produce classical cytokines, mainly including IL-17A and IL-22, to mediate the pathological progress of the inflamed intestine.20,21,24 In this study, for the first time, we linked the role of BAs and ILC3s in colitis and found that the 12-KLCA-induced improvement of colitis was associated with the preferential suppression of ILC3s secreting IL-17A, but not IL-22. Here, IL22 is linked to colitis.