Upon stimulation in inflammatory conditions such as in rheumatoid arthritis by inflammatory cytokines, the IκB kinase (IKK) complex phosphorylates IκBα for subsequent ubiquitination and proteasome-mediated degradation, and IκBα dissociation induces NF-κB p65 subunit localization to the nucleus and binding to specific gene promoters to regulate pro- and anti-inflammatory protein expression. This evidence concerns the gene NFKB1 and rheumatoid arthritis.