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]. The gene discussed is NFKB1; the disease is rheumatoid arthritis.