The dysfunctional NCF1‐339 allele, which impairs the function of the NOX2 complex, is the major genetic association for SLE, with regards to odds ratio and allelic frequency.[51, 52] Dysfunctional NCF1 affects ROS production and is strongly associated with SLE in humans and mouse models.[12] Our previous study has found pDCs as the key immune cell type driving SLE pathogenesis.[12] ROS deficiency enhances the generation, accumulation, and function of pDCs, which exacerbates pristane‐induced and spontaneous lupus. This evidence concerns the gene CYBB and systemic lupus erythematosus.