It has been long known that intestinal inflammation is central for the pathology that follows infection with non-typhoidal Salmonellae such as Salmonella Typhimurium. However, in recent years work carried out in the laboratories of Wolf-Dietrich Hardt and Andreas Baumler have established that the inflammatory response is also required for Salmonella Typhimurium to compete with the resident intestinal microbiota and to secure essential nutrients. Unlike most other tissues, where the mere presence of bacterial products capable of stimulating innate immune receptors can trigger inflammation, the intestinal tract presents a challenge to those pathogens that need inflammation to sustain their livelihood. Indeed, the presence in the intestinal tract of an abundance of microbial products with the potential to stimulate innate immune receptors demands for the intestinal epithelium to be subject to negative regulatory mechanisms that can prevent the pathology that could result from the indiscriminate firing of these receptors. In fact, misregulation of those mechanisms can result in chronic inflammatory conditions such as inflammatory bowel disease. Consequently, to initiate an inflammatory response in the gut, S. Typhimurium cannot relay on the stimulation of innate immune receptors by the standard “pathogen-associated molecular patterns” (e. g LPS, peptidoglycan, flagellin) that, like many other bacteria, posses in abundance. Therefore, the mechanisms by which Salmonella trigger intestinal inflammation have been a long-standing question in the field and have been the subject of some controversy. We believe that a paper that we recently published in Nature Microbiology has finally clarified this important issue.