As observed in the current study results, the maintenance of a band-like lymphocytic inflammatory infiltrate across the entire corium-epithelial junction, as is observed in OLP, OLR, and other autoimmune diseases, may be associated with the overexpression of the bcl-2 protein and the capacity that it imprints on these cells to maintain an inflammatory response without undergoing apoptosis. This evidence concerns the gene BCL2 and autoimmune disease.