The clinical and legal implications regarding the association between the antibiotics exposure and the risk of type 2 diabetes mellitus reported from a population from the United Kingdom (1) requires more research because of its magnitude and significance for the health system, patients, and physician. This noncausal association demands a concerted effort to determine whether the antibiotics may induce the development of diabetes. Furthermore, similar results were observed in a Danish population (2). Therefore, this scenario proposes the development of new hypotheses; the prolonged exposure to antibiotics affects the environment of the gut microbiota. The changes in gut microbiota may influence the metabolic pathways related to the pathogenesis of components of metabolic syndromes such as obesity, insulin resistance, hypertension, dyslipidemias, and diabetes. Evidence suggests that microbiota and its derivatives act as cofactors in transfer reactions that can contribute to DNA methylation (3) and induce the stimulation of regulatory cytokines and mediators (such as IL-4, IL-5, IL-10, IL-13, and TGFβ) to maintain the healthy balance of the intestinal mucosa (4) as an epigenetic regulation mechanism. Another proposed mechanism is an increased permeability of the intestinal epithelium that may lead to increased absorption of macromolecules from the intestinal content, resulting in systemic immune responses, low-grade inflammation, and altered signaling pathways influencing lipid and glucose metabolism (5).