Multiple complement components, regulators, complement activation products, and inflammatory proteins have been identified to be upregulated in AMD conditions, including C3, C3d; the terminal components C5, C6, C7, C8, and C9; terminal complement regulators vitronectin and clusterin, apolipoproteins apoA1, apoA4, and apoE; as well as thrombospondin, serum amyloid A (SAP-A), and SAP-P [23, 40]. This evidence concerns the gene APOA4 and age-related macular degeneration.