Whether crosslinks between the AP-1 pathway and other central signaling pathways [e.g., mitogen-activated protein kinases (MAPK; such as JNK, extracellular signal-regulated protein kinase (ERK), and p38), the phosphatidylinositide-3-kinase, and the Janus kinase/Signal transducer and activator of transcription (Jak/STAT) pathway [45,46,47]], known to be dysregulated in RA [46,48] and other diseases [49,50], contribute to the aforementioned differences, remains the focus of future studies. This evidence concerns the gene FOS and rheumatoid arthritis.