Lipoprotein(a)-induced atherosclerosis is mediated via various mechanisms including, but not limited to, structural homology to plasminogen resulting in high-affinity binding to fibrinogen and inhibition of plasminogen activation; pro-inflammatory effects resulting in recruitment of inflammatory cells to site of atherosclerosis; inhibition of TGF-β activation; oxidation of Lp(a); and migration and proliferation of smooth muscle cells and endothelial cells [24]. The gene discussed is PLG; the disease is atherosclerosis.