Using a wire injury-based accelerated atherosclerosis model, we demonstrate that FcγrIII deficiency reduces neointimal plaque size and macrophage content and induces a stable plaque phenotype with an increased VSMC compartment, which was paralleled by reductions in proinflammatory cytokine TNF-α, the chemokine MCP-1/CCL2, and the atherogenic adhesion molecule VCAM-1 in the vasculature. The gene discussed is CCL2; the disease is atherosclerosis.