Regulatory T cells (Treg) play a key role in tolerance and immune homeostasis. Our research has revealed that Treg function and stability is orchestrated by gene networks regulated by FOXP3 and microRNAs. It is now evident that coordinated gene regulation occurs in a cell specific manner to bring together regulatory elements and coding regions, and this is conformation dependant. While bioinformatics can predict targets of transcription factors with some accuracy, and genomics datasets can now identify functional motifs in chromatin, such as super enhancers and lncRNAs, the targets of these regions cannot be predicted by linear annotation models. We have established conformation capture in order to determine which non coding elements interact with Treg specific genes, and to superimpose on this our FOXP3 binding site data. This analysis will reveal the conformation dependant transcriptional regulation of Treg genes, and will also allow for the first time annotation of SNPs from autoimmune diseases to functional targets. This approach will shed light on the 80% of SNPs that do not disrupt a coding region, and whose targets are currently unknown. As proof of principle we have used SATB1, a key FOXP3 repressed gene in Treg (1), as a conformation capture target. Using 4Cseq we have identified a T cell specific activation induced FOXP3 responsive super enhancer over 300Kb upstream, and this region includes 4 enhancer elements.  We now confirm that this enhancer is T cell activation dependant, is repressed by FOXP3, and overlaps a number of IBD/Colitis SNPs from GWAS datasets, confirming the power of this approach. The functional impact of autoimmune SNPs that map to this region on SATB1 expression is now under investigation.