Whereas the pathogenesis of IBD is generally believed to be the result of immune dysregulation due to the interaction of genetic and microbial factors, this stimulus will also accelerate cellular senescence and promote increased production of inflammatory factors such as tumor necrosis factor (TNF) α, interleukin (IL)-1, IL-6, IL-18, IL-12 and IL-23 [30–32]. The gene discussed is IL18; the disease is inflammatory bowel disease.