Furthermore, acidity drives pro-inflammatory gene expression in infiltrating immune cells through multiple acid-sensing mechanisms,9,10 with emerging evidence suggesting that the upregulation and increased activity of proton-sensing G protein-coupled receptors (GPCRs), such as G protein-coupled receptor 68 (GPR68), contribute to these changes in immune cell behaviour and ultimately the pathogenesis of IBD.7 This evidence concerns the gene GPR68 and inflammatory bowel disease.