Yen et al. used IL-10 knockout mice, a spontaneous IBD model, and showed that the development of colitis was suppressed by IL-23p19 deficiency but not IL-12p35 deficiency in IL-10−/− mice; administration of IL-23 accelerated the onset of colitis and promoted inflammation through IL-17- and IL-6-dependent mechanisms [36]. The gene discussed is IL17A; the disease is inflammatory bowel disease.