Additionally, in colitis models, Flt3L treatment preferentially led to the expansion of CD103+ DCs and Tregs, alleviating Crohn’s-like murine ileitis [25], whereas in another study, CD103+ DCs favored the emergence of interferon-γ (IFN-γ)-producing CD4+ T cells, thereby abrogating tolerogenic properties [26]. The gene discussed is ITGAE; the disease is colitis.