The vast majority of 5-HT is detected in the gastrointestinal epithelium and is produced by enterochromaffin cells of the gut mucosa. The 5-HT7R contributes in generation/perturbation of intestinal inflammation [36]. 5-HT7R expression is significantly increased in inflamed intestinal dendritic cells of patients with Crohn’s disease as well as in an experimental murine models of inflammatory bowel disease such as DSS-induced colitis [37]. However, the testing of the involvement of 5-HT7R in pathological gastrointestinal functions has produced contradictory results that depend on the experimental model used. Specifically, pharmacological antagonism or genetic ablation of 5-HT7R resulted in increased severity of symptoms in both acute and chronic mouse models of colitis. Consistent with the 5-HT7R endogenously restraining the pathology of this disease, activation of the receptor by agonists produced an anti-inflammatory effect [38]. In stark contrast, Kim and collaborators showed that genetic or pharmacological silencing of 5-HT7R reduced the severity of intestinal inflammation after induction of colitis in mice [39]. As in CNS disorders and CV disease described above, the consortium could help understanding these contradictory results by gathering the experts and information around the 5-HT7R (proposed below).