Celiac disease is sustained by an immunological process that mainly affects the jejunal mucosa (1 ). Nonetheless, jejunum is not the only site of the gastrointestinal tract that is involved in celiac disease. In recent years, Ensari and colleagues (2 ,3 ), by using immunohistochemical analysis and computerized image analysis for numerical quantitation, have significantly contributed to a definitive and clear demonstration of a celiac disease-associated “proctitis,” and its gluten dependence. Morphometry has shown increased populations of plasma cells, lymphocytes, and mast cells in the rectal mucosa of untreated patients, with these changes being reverted, with the sole exception of mast cells, by dietary treatment (2 ). The immunohistochemical approach has demonstrated highly significant increases in CD3+ and γδ+ lymphocytes within both the lamina propria and the epithelium. Mononuclear cells, both lymphocytes (CD3+ ) and macrophages (CD68+ ) expressing interleukin-2 (IL-2) receptors (CD25+ ), have been found to be increased in the lamina propria, usually immediately below the basal lamina. Enterocytes have been noted to be positive for major histocompatibility complex class II display, a pattern usually absent in normal colon. Furthermore, increased expression of vascular cell adhesion molecule-1 (VCAM-1) molecules in the rectal mucosa of untreated, compared to either treated celiac rectum or control mucosae, has been reported (3 ). As a whole, these data suggest, analogously to jeunum, an ongoing T-cell-dependent, cell-mediated immune response in the rectal mucosa.