For example, an enhancer harboring GWAS risk variants for rheumatoid arthritis was identified between oligodendrocyte transcription factor 3 (OLIG3) and TNFAIP3. In contrast to the well characterized role of TNFAIP3 in regulating inflammatory signaling pathways, OLIG3 is an important regulator of neuronal development and has no established role in the immune system [58], suggesting that TNFAIP3 was the likely target of this enhancer. This evidence concerns the gene OLIG3 and rheumatoid arthritis.