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. Here, ADAM3A is linked to systemic lupus erythematosus.