By integrating linkage disequilibrium patterns, QTL fine-mapping results, and allele-specific chromatin accessibility information from AFGR, we reduced a GWAS region of 28 equally prioritized credible set variants in perfect LD to a single candidate variant, and identified a potential molecular mechanism by which that variant may impact multiple sclerosis risk through transcription factor binding regulation of IL7 gene expression. Here, IL7 is linked to multiple sclerosis.