In RA pathogenesis, dysregulated NF-kB signaling contributes to the activation of both immune and non-immune cells through the transcriptional regulation of inflammatory mediators, including TNF-α; IL-1, -2, -6, -8, -9, -12, -18, and -23; GM-CSF; VEGF; RANKL; MCP-1; MIP-2; CXCL1; CXCL10; RANTES; ICAM-1; VCAM-1; MMPs; and COX-2 [27]. This evidence concerns the gene CSF2 and rheumatoid arthritis.