Celiac disease (gluten enteropathy) is a chronic autoimmune disease. It is characterized by gluten intolerance in genetically predisposed persons. Gluten generates an autoimmune response within the small intestine wall, causing damage that results in malabsorption. The small intestine damage is most noticeable in jejunum. Intestinal villi are absent, and intestinal crypts are hypertrophic, leading to flattened and reduced absorption surface of the small intestine. Disease has a diverse clinical picture, may manifest at any age, and severe complications may occur if not treated. The key genetic factor of the disease is the human leukocyte antigen system, but there is a large number of genes outside the region that contribute to the pathogenesis of the disease, and are only partly shared by some patients, indicating the genetic heterogeneity of the disease. In addition, it has been found that many of these risky loci in the celiac are commonly associated with locus for other autoimmune diseases. Contemporary serological tests are specific and sensitive, but small intestinal mucosa biopsy is still a "gold standard" in diagnosing, so it is necessary to combine multiple serological tests with histological findings of the small intestine mucosa biopsy. Illness can only be treated with lifelong gluten-free diet. Education is crucial to successfully treating patients. Untreated patients have a higher health risk than patients who properly adhere to the gluten-free diet. Apart from celiac disease, gluten can cause another two disorders: allergies and gluten sensitivity.