Inflammatory bowel diseases (IBD) are chronic debilitating diseases affecting young subjects and inducing an alteration of the quality of life. Pathogenesis of IBD is not fully understood but the current hypothesis is an inappropriate activation of the gastrointestinal immune system toward the gut microbiota in genetically susceptible hosts and under the influence of environment. Until now, most of the therapeutic strategies used have targeted the host immune system only but unfortunately no cure has been found and there is room for improvement. There are many arguments regarding the potential use of the gut microbiota as a therapeutic target. Among them, we can cite the role of the fecal stream in postoperative recurrence of Crohn’s disease, the need for a microbiota to trigger inflammation in animal model of colitis, the association of polymorphisms in genes involved in microbial sensing with IBD and the abnormal composition of the gut microbiota in IBD patients. This imbalance in the composition of gut microbiota is named dysbiosis. It has notably been shown that the level of bacteria with pro-inflammatory potential is increased whereas the one of anti-inflammatory potential is decreased. As an example, Faecalibacterium prausnitzii, one of the most prevalent bacteria of the normal human gut microbiota, is decreased in IBD patients and has been shown to have anti-inflammatory effects in vitro and in vivo. Indeed, some existing studies using antibiotics or probiotics suggest that the gut microbiota is a good target, and new strategies using fecal microbiota transplantation are promising although still in evaluation. Finally, the gut microbiota might also be useful as a biomarker in IBD as modifications in the gut microbiota have been shown to predict clinical events.