Similar to our findings, mice lacking CD103+CD11b− DCs do not exhibit signs of spontaneous inflammation in the steady state34, 35, but their susceptibility to DSS-induced colitis seems to vary depending on additional factors: models using deficiency in the transcription factor BATF3 to induce CD103+CD11b− DC deficiency are as susceptible as their wild-type counterparts34, while employing diphtheria-toxin-mediated ablation of CD103+CD11b− DCs in Clec9A-DTR mice renders them significantly more sensitive to induced colitis35. The gene discussed is ITGAE; the disease is colitis.