It had previously been reported that RA is characterized by an excess of proinflammatory cytokines, as well as a deficit in muscle mass, so these causes were investigated in an in vitro study, which found that myostatin regulated IL-1β expression through the transduction pathways of extracellular signal-regulated kinase (ERK), mitogen-activated protein kinases (JNK), and activating protein-1 (AP-1) signals [74]. This evidence concerns the gene IL1B and rheumatoid arthritis.