The introduction of anti-TNF therapy has dramatically improved the outlook for 
patients suffering from a number of inflammatory conditions including rheumatoid 
arthritis and inflammatory bowel disease. Despite this, a substantial proportion 
of patients (approximately 30-40%) fail to respond to these potentially toxic 
and expensive therapies. Treatment response is likely to be multifactorial; 
however, variation in genes or their expression may identify those most likely 
to respond. By targeted testing of variants within candidate genes, potential 
predictors of anti-TNF response have been reported; however, very few markers 
have replicated consistently between studies. Emerging genome-wide association 
studies suggest that there may be a number of genes with modest effects on 
treatment response rather than a few genes of large effect. Other potential 
serum biomarkers of response have also been explored including cytokines and 
autoantibodies, with antibodies developing to the anti-TNF drugs themselves 
being correlated with treatment failure.