Abdominal pain is a leading cause of morbidity in gastrointestinal disease. Despite this we still know little of how pain is triggered in ?functional? gastrointestinal disorders such as irritable bowel syndrome (IBS) and gastrointestinal diseases such as inflammatory bowel disease (IBD). Work from my lab uses normal and diseased human tissue to determine the mediators responsible for the activation of pain sensing nerves (nociceptors) in IBS and iBD patients, and the mechanism by which they activate nociceptors. Recent studies have identified a critical role for the voltage gated sodium channel subtype NaV1.9 in the activation of visceral nociceptors in IBD, and a key role for proteases in visceral nociception.