The key role of the NF-κB signaling pathway in SLE pathogenesis is well known; it controls the survival and proliferation of autoreactive T and B cells, but also regulates the inflammatory response by modulating the expression of pro-inflammatory mediators such as Th1/Th17 cytokines and the enzymes COX-2 and iNOs [58]. This evidence concerns the gene NFKB1 and systemic lupus erythematosus.