As NF-κB acts as a pivotal regulator of pro-inflammatory molecules, such as tumor necrosis factor (TNF)-α and interleukin (IL)-6, in the pathogenesis of RA [9, 10], we hypothesized that O-GlcNAcylation of NF-κB might affect the course of RA. This evidence concerns the gene NFKB1 and rheumatoid arthritis.