Since SLE causal variants at FAM167A-BLK are very likely to be in the BLK promoter region (see discussion in Introduction) and given our findings above, we hypothesized that these variants may have functional effects on modulating FAM167A expression, and on disease risk, via haplotype-specific chromatin interaction between promoters of BLK and FAM167A. We thus sought to perturb BLK expression and measure changes in FAM167A expression. This evidence concerns the gene BLK and systemic lupus erythematosus.