Those capabilities can be extremely significant in RA because IL-1 activity leads to stimulation of cells (especially of synovial fibroblasts), increasing production of cytokines, chemokines, and inducible nitric oxide synthase (iNOS), prostaglandins, MMPs, GM-CSF [74,76,77], and adhesion molecules of endothelial cells [78]. This evidence concerns the gene CSF2 and rheumatoid arthritis.