Despite the efficacy of eliminating celiac disease's environmental stimulus (gluten), persistent attention to a hereditary predisposition makes the disease an intriguing model for exploring environment–heredity interactions in the production of autoimmune disease. Although celiac disease has been recognized as an autoimmune condition for several decades, its expression or course, being easily modified, does not conform to what we expect of such pathogenic processes. In celiac disease, unlike most other autoimmune conditions, the environmental trigger that sets off the immunologic disorder is readily identified — and can be avoided. Indeed, long before autoimmune causation was recognized, we knew that altering a person's diet sometimes prevented or arrested the disease. For the past hundred years, physicians have recommended various dietary adjustments, some more effective than others, to modulate the expression of celiac disease, or . . .