In the context of SLE, the inflammatory environment can lead to the release of IL-6 or TNF-α, which activate the NF-κB pathway.349 This activation enhances the activity of the miR-34a promoter, resulting in the downregulation of Foxp3 expression and excessive proliferation of T cells.350 Additionally, NF-κB has been shown to be upregulated in autoreactive B cells mediated by CD40 and BAFF, promoting the secretion of autoantibodies.351,352 Furthermore, IFN-1 is a key factor in the pathogenesis of SLE, and its induction is mediated by NF-κB activation through TLR7 stimulation.353. The gene discussed is IL6; the disease is systemic lupus erythematosus.