Celiac disease (CD) is an autoimmune disorder triggered by gluten in genetically susceptible individuals characterized by a variable combination of gluten-dependent symptoms, presence of specific autoantibodies and enteropathy. The health burden of CD is considerable, as it reduces quality of life  and, at a societal level, has extensive negative economic consequences. Prevention strategies are based on the identification of at-risk subjects and identification and elimination of risk factors. A number of prospective observational and interventional studies conducted on the general population, and more often in subjects at-risk, have given important information on the natural history of the disease. Both genetic and environmental factors have been identified with the former, in particular histocompatibility genes, playing a major role. Environmental factors, some operating already before birth, have been identified, with feeding pattern in the first year of life (breast feeding, amount and time of introduction of gluten) and infections being the most relevant. Prospective studies have also allowed the identification of biomarkers predictive of the disease which in perspective could better define the population on which to intervene. Interventions have been so far limited to modifications of feeding patterns. However, as also learnt from diseases that share with CD genetic risk factors and mechanisms of damage, such as type 1 diabetes (T1D), future strategies may be envisaged based on protection from infections, manipulation of microbiota, intervention on T cells.