Myeloid-specific Iκκ-β (an activator of NF-κB)-deficient mice have shown decreased NF-κB activation and pro-inflammatory cytokine production (IL-1β, IL-6, TNF-α, and MCP-1), leading to inhibition of the development of insulin resistance (Arkan et al., 2005). This evidence concerns the gene CCL2 and Insulin resistance.