AGEs are known to accumulate in certain diseases involving a chronic state of inflammation (such as cardiovascular (CV) disease, diabetes mellitus (DM), chronic renal failure, Alzheimer’s and more recently rheumatic illnesses like rheumatoid arthritis (RA) or SLE), stimulating the AGE receptors (RAGEs) and therefore causing an amplification of the already present inflammation through production of type 1 interferon, tumor necrosis factor α, and/or interleukin 6 via intracellular activation of the NF-KB pathway [11,12,13,14]. This evidence concerns the gene NFKB1 and rheumatoid arthritis.