In addition, I recently pointed out to the best of my knowledge, which was also confirmed by a literature search using the PubMed database, that there have yet to be any RA clinical trials which have employed strategies designed to increase SOCS-based regulation of JAK/STAT signaling, although Shouda et al. [47] had predicted that over-expressing SOCS3 in RA synovial tissue might have clinical benefit by dampening the clinical symptoms of RA. This evidence concerns the gene SOAT1 and rheumatoid arthritis.