IL6 and rheumatoid arthritis: Many of these immune cells and their mediators, known to be relevant in the pathogenesis of RA [3], have become target of highly specific therapeutic options, directed against mediators (e.g., TNF-alpha, IL-6), immune cells (e.g., CD20 B cells), and, more recently, intracellular signaling pathways (e.g., Jak-Stat pathway inhibitors) [4].