In RA, a deregulated NF-κB signaling pathway contributes to the pathogenic process and activates both immune and non-immune cells (e.g., FLS) through transcriptional regulation of inflammatory mediators, including TNF, IL-1, IL-2, IL-6, IL-8, IL-9, IL-12, IL-18, IL-23, GM-CSF, VEGF, RANKL, MCP-1, MIP-2, CXCL1, CXCL10, RANTES, ICAM-1, VCAM-1, MMPs, and COX-2. This evidence concerns the gene CCL5 and rheumatoid arthritis.