Once activated, NF-κB suppresses type II collagen synthesis and increases the production of matrix metalloproteinases, aggrecanases, and various chemokines—including IL-8, monocyte chemoattractant protein-1 (MCP-1/CCL2), CCL5, and macrophage inflammatory protein-1α (MIP-1α)—which further attract inflammatory cells and intensify joint inflammation [42]. The gene discussed is CCL3; the disease is Arthritis.