Interestingly, IL-23 could also act via intestinal epithelial cells, inducing the c-type lectin RegIIIβ-mediated recruitment of IL-22-producing cells, and in the absence of this signaling (Il23rflox/floxVillin-Cre), mice were susceptible to DSS colitis and were characterized by dysbiosis [237]. The gene discussed is IL37; the disease is colitis.