In MS, clinical therapies aimed to block TNF-α-mediated pro-inflammatory effects (Van Oosten et al., 1996; The Lenercept Multiple Sclerosis Study Group and The University of British Columbia MS/MRI Analysis Group, 1999; Sicotte and Voskuhl, 2001) did not yield in an amelioration of disease and even worsened the clinical course in some patients, strongly suggesting a bivalent role of TNF-α in demyelination and myelinogenesis. The gene discussed is TNF; the disease is myeloid sarcoma.