Hydrogen sulfide (H₂S) is produced by sulfate-reducing bacteria present in the colon. Recently, it has been demonstrated that mammals have enzymatic pathways to produce H₂S. As H₂S was added to the list of gaseous signaling molecules, the number of papers related to H₂S biology has increased exponentially. However, the physiological role of H₂S in the gastrointestinal tract is still unknown. Endogenous production in different cell types indicates that H₂S might participate in various functions such as pain, motility and secretion. Nevertheless, experimental protocols to demonstrate a physiological role for H₂S are not easy to perform due to the lack of specific antagonists. Genetically modified animals lacking a specific route of H₂S synthesis are useful biological tools although whether they alter gastrointestinal function are still unknown. In this issue of Neurogastroenterology and Motility, Krueger et al. examine the role of H₂S in secretion and in afferent neuronal activation using sodium hydrosulfide as a source of H2S. Interestingly, sodium hydrosulfide causes secretion and increased spike activity in afferent neurons. The mechanism partly involves transient receptor potential vanilloid type I located on afferent neurons, causing local release of substance P, which in turn activates cholinergic secretomotor neurons. These novel observations extend our understanding of the function of H₂S in the gastrointestinal tract.