The mechanisms by which Lp(a) may cause atherosclerosis and cardiovascular risk are based on the induction of adhesion molecules, which are VCAM-1, ICAM-1, and also proinflammatory chemokines (MCP-1) found in endothelial cells; foam cell formation due to Lp(a) uptake in macrophages; and proinflammatory production of IL-8 along with reduced expression of inducible nitric oxide synthase (iNOS). The gene discussed is ICAM1; the disease is atherosclerosis.