Since anti-TNF therapy for Crohn’s disease and rheumatoid arthritis (conditions not known to be linked to MS) have been reported to precipitate subsequent demyelination [85-88], low levels of TNF per se, whether due to TNF blockade or genetic factors, may be the major risk for demyelination [89], and systemic anti-TNF therapy for IIU might present the same risk. The gene discussed is TNF; the disease is Crohn disease.