Several studies support the hypothesis of a potential involvement of Wnt signaling in the etiology of RA, in particular Wnt7b [20]: higher levels of Wnt ligands, Frizzled receptors, and Wnt inducible signaling pathway proteins were observed in the synovium of RA patients, also as pro-inflammatory cytokines TNFα, IL-1β and IL-6. This evidence concerns the gene TNF and rheumatoid arthritis.