The authors found that, in the RA model, TLR2 receptor activation induced metabolic changes in RA synovial fibroblasts (RASFC), leading to proinflammatory cytokine production, cell migration/invasion, and the transcriptional upregulation of nuclear factor kappa B (NF-κB) and STAT3 phosphorylation [85]. This evidence concerns the gene STAT3 and rheumatoid arthritis.