In fact, based on these findings, using the TNF-α or IL-6 receptor blockade to achieve clinical remission in active RA patients would be predicted to shut down STAT protein activation even though blockade of TNF-α or IL-6 would also likely involve their more conventional site of action on signal transduction, namely the Stress-Activated/Mitogen-Activated Protein Kinase (SAPK/MAPK) pathway [21,22,23]. This evidence concerns the gene IL6 and rheumatoid arthritis.