Furthermore, Nrf2 and Keap1 levels decreased in pDCs from patients with active SLE compared to healthy controls, suggesting that regulation of oxidative stress via the Keap1/Nrf2 pathway was impaired in pDCs in these patients [74], which may contribute to the pathogenic role of pDCs in SLE. This evidence concerns the gene NFE2L2 and systemic lupus erythematosus.