The cylindromatosis (CYLD) gene was originally identified as a tumor suppressor that is mutated in familial cylindromatosis, an autosomal dominant condition that confers a predisposition to multiple tumors of the skin appendages. CYLD has deubiquitinating enzyme activity and inhibits the activation of transcription factor NF-kappaB. Therefore, loss of CYLD function correlates with tumorigenesis. Expression of CYLD has been detected in various organs, but its expression in salivary gland tumor (SGT) is still unknown. Adenoid cystic carcinoma (ACC) is a well known and typical malignant SGT ACC was previously known as cylindroma in view of its marked histological resemblance to dermal cylindroma. In this study, the expressions of CYLD and NF-kappaB mRNA in HSG, a human SGT cell line, were found to be increased by TNF-alpha stimulation. Immunohistochemistry clearly demonstrated the expression of CYLD and NF-kappaB-related factors in ACC tissue.