This fascinating article1 presents a novel hypothesis and interpretation of observed data combining bench research and clinical experience. The basic premise of the hypothesis is that the presence of an intact vagus nerve and gut innervations will decrease the postinjury inflammatory response and that patients who happen to have had a vagotomy sometime during their admission for a traumatic injury will have worse inflammatory-mediated outcomes. The basic science supporting the importance of an intact vagal signal in downregulating the inflammatory response, particularly decreasing intestinal permeability, is well referenced. Peterson et al have done a nice job of using the NIS database to test this hypothesis, identifying trauma patients who had a vagotomy and matching them as best as possible to a similar cohort who did not have a vagotomy but had similar demographics and injury severity pattern. There certainly are problems with this approach, but these are clearly stated in the “Comments” section. As far as I know, this is a novel look at the role of vagotomy and outcome in injured patients. However, the basic criticism of this article is that the higher incidence of inflammatory-mediated adverse outcomes (ARDS, SIRS/sepsis, septicemia) and hospital mortality is not the result of the vagotomy disinhibiting the inflammatory response but rather a consequence of severe injury, gut ischemia, development of a gastrointestinal ulcer and bleeding, and the subsequent necessity for gastrectomy and vagotomy. Peterson et al acknowledge this and made an effort to control for it, primarily by adjusting for the comorbidity of ulcer disease, but this was not particularly effective. Nonetheless, the article is well written, concise, creative, and consistent with previous study by some of the authors. I suspect it will be educational to many readers, and while seriously flawed, Peterson et al are very clear on this and not overreaching in their discussion and conclusions.