However, recent transgenic approaches to dissect the contribution of NCR+ versus LTi-like ILC3-derived IL-22 in response to this pathogen have suggested NCR+ ILC3-derived cytokine is likely not required to control bacterial load [33, 34], in line with the dominance of LTi-like ILC3 in the colon—the site of infection—and previous reports suggesting LTi-like ILC3-derived IL-22 is critical in this model [28]. Here, IL22 is linked to infection.