Given that acid-sensing is a conserved function of pain sensing neurons across species and a defining feature of polymodal nociceptors, facilitated by their expression of acid-sensitive ion channels and GPCRs,27 we sought to understand whether proton-sensing GPCRs such as GPR68 might also be responsible for the activation of colonic nociceptors by acid, and as such contribute to the activation of both nerve endings and immune cells following acidification of the bowel in individuals with colitis. This evidence concerns the gene GPR68 and colitis.