However, in agreement with our expectations we observed that ADAM3A duplication was statistically lower in SLE patients than in controls (p = 1.23 x 10−2, OR = 0.2 [95% IC, 0.1–0.7]) (S4 Fig), suggesting that gains in the ADAM3A gene are a protective factor for the development of SLE. This evidence concerns the gene ADAM3A and systemic lupus erythematosus.