computational approaches can help to identify the targets of enhancer-risk variants. The method developed by Thurman and colleagues was applied to all GWAS loci and predicted gene targets of 419 disease-associated risk variants [20], most of which were located more than 100 kb from the risk SNP. PreSTIGE was utilized to predict gene targets of 122 noncoding loci associated with six immune disorders: rheumatoid arthritis, Crohn’s disease, celiac disease, multiple sclerosis, lupus and ulcerative colitis. Furthermore, at several of the autoimmune-disease-associated loci, the effect of the risk allele on target gene expression was quantified.
