Type 1 diabetes is an autoimmune disease that results in a progressive (complete in most cases) destruction of insulin-secreting beta cells from Langerhans islets. Even if the autoimmune process becomes to be well known, no one is yet sure what specifically prompts the autoimmune response that destroys the body's ability to produce insulin. Etiology of this complex disease combines a genetic predisposition and still (almost) unknown environmental factors that trigger autoimmuninty specifically targeting beta cells. Genetic HLA predispositions are clearly identified. However, only few people with apparent genetic predisposition to type 1 diabetes actually end up getting the disease. Moreover, the remarkable increase of type 1 diabetes prevalence observed in numerous countries can not be explained by genetics. Because genetic factors can't predict alone the development of type 1 diabetes, environmental factors must be involved such as viral infections, toxins from food, cow milk during childhood (instead of breast feeding) or vitamin D deficiency. This paper aims at describing the role of the genetic predisposition and the environmental hypothesis which can be involved in the development of type 1 diabetes. We will conclude by briefly describing clinical trials targeting either the immune response or the potentially toxic environment.