These immune cells release various sensitizing mediators, such as prostaglandins, substance P, and nerve growth factor, which can in turn provide a peripheral mechanism of sensitization of spinal nociceptive pathways, and their increased numbers in IBS patients may contribute to visceral hypersensitivity, shown to be correlated with abdominal pain and altered colonic motility [20, 21]. The gene discussed is TAC1; the disease is irritable bowel syndrome.