OxPL is proven to play a major role in arterial inflammation induced by lp(a), as it could predispose in the vessel wall, promote monocyte infiltration, and increase the secretion of pro-inflammatory cytokines (e.g., interleukin (IL)-8, monocyte chemoattractant protein-1), causing endothelial dysfunction, lipid accumulation, and regional inflammation within coronary plaques [4,15]. The gene discussed is CCL2; the disease is endothelial dysfunction.