Notably, it is now widely accepted that IL-23, predominantly produced by activated dendritic cells in response to both pathogenic and nonpathogenic bacteria [26,27,28], plays a fundamental role—together with IL-1β—in the differentiation and maintenance of pathogenic Th17 cells, in turn contributing to the pathogenesis of IBD [29,30]. The gene discussed is IL23A; the disease is inflammatory bowel disease.