The proatherogenic effect of Th1 cells in atherosclerosis appears to involve an important role for the chemokine receptor CCR5, a well-known HIV-1 co-receptor, through the T cell recruiting action and other effects of its ligands: macrophage inflammatory protein 1α (MIP-1α, CCL3), MIP-1β (CCL4), and RANTES (regulated on activation normal T cell expressed and secreted, CCL5) [348]. The gene discussed is CCL3; the disease is atherosclerosis.