Even though the etiopathogenesis of IBD remains not completely understood, there is growing evidence that increased infiltration, proliferation, and activation of Th17 cells and increased concentrations of IL-23/Th17 pathway proinflammatory cytokines including, inter alia, tumor necrosis factor α (TNF-α), interleukin 23 (IL-23), interleukin 17 (IL-17), and chemerin play a pivotal role in the development and maintenance of mucosal inflammation and lead to gut tissue damage. The gene discussed is RARRES2; the disease is inflammatory bowel disease.