Tumor necrosis factor (TNF) is well documented as a pleiotropic mediator with a wide range of biological functions.1 It is selectively toxic to some tumor cells in vivo and in vitro,2 which leads to the ongoing interest in the potential clinical value of TNF as a tumoricidal agent. In this study, we explored the cellular source of TNF mRNA and the relationship between the expressions of TNF mRNA, TNF protein, and TNF receptor (TNFR) protein products in cervical lesions.