AbstractAlmost all of Genome Wide Association Studies (GWAS) hits come from non-coding DNA elements. Data from chromatin interaction analyses suggest a long-range interaction with a putative enhancer upstream ofTNFAIP3. Disrupting the enhancer may impairTNFAIP3expression and enhance SLE risk. Two variants, rs10499197 and rs58905141 carried on the SLE risk haplotype are situated near this enhancer and could affect its function. Cloning the regulatory region surrounding rs10499197 into an expression plasmid containing a CRISPR-Cas9 backbone, and then performing a genome editing assay, we found that the variant is located near an enhancer. And any changes to the SNP region might impair enhancer and its ability to regulateTNFAIP3expression.