Interleukin-1 (IL-1), interferon-γ (IFN-γ), and tumor necrosis factor-α (TNF-α) were among the pro-inflammatory cytokines that were reduced by blocking FKN-CX3CR1 interaction, suggesting that this pathway could be a target for the therapy of rheumatoid arthritis [69]. This evidence concerns the gene TNF and rheumatoid arthritis.