In myeloid-specific Iκκ-β (an activator of NF-κB)-deficient mice, a decrease in proinflammatory cytokine production (IL-1β, IL-6, TNF-α, and MCP-1) and the inhibition of NF-κB activation has been reported, avoiding, in this way, the development of insulin resistance [75]. This evidence concerns the gene CCL2 and Insulin resistance.