Celiac disease provides a unique model for autoimmune research because the following key elements are known: the specific genes involved in its pathogenesis and the environmental trigger. Substantial genetic research has uncovered the strong influence of the HLA antigen and its mechanistic role in presenting deamidated gluten to effector immune cells involved in the pathogenesis of celiac disease. Researchers also have identified more than 57 alleles in addition to HLA genes that confer risk.1 Although this information is crucial to understanding celiac disease, it cannot explain the substantial increase in the prevalence of celiac disease from 0.21% to 0.95% in the United States2,3 between 1974 and 2003 or in celiac disease incidence from 5.2 (95% CI, 3.8-6.8) per 100 000 person-years to 19.1 (95% CI, 17.8-20.5) per 100 000 person-years (incident rate ratio, 3.6; 95% CI, 2.7-4.8) in Europe between 1990 and 2011.4 Thus, there is substantial interest in the environmental trigger, gluten, particularly related to the timing of its introduction and amount ingested as the driving factors associated with this increased prevalence.