Tumor necrosis factor is a cytokine with a range of functions, including induction of fever, defense against pathogens, inflammation, immune regulation, inhibition of tumor growth, stimulation of vascular endothelium, and proliferation of immune cells.42 Proposed mechanisms for the paradoxical development of inflammatory CNS events in association with TNF inhibitor exposure include immune dysregulation from the inhibition of apoptosis of autoreactive T cells, which may then enter the CNS and cause demyelination.43 TNF inhibition may result in upregulation of TNF expression. The gene discussed is TNF; the disease is neoplasm.