Despite the long road of discovery that lies ahead, various lines of evidence linking the AP to AMD disease pathogenesis including (a) clinical phenotypes that associate with deficiencies of AP regulators [119]; (b) linkage of SNPs in AP components to disease risk [11, 120]; and (c) the functional analysis of individual AP components in the establishment of clinical phenotypes observed in both mouse and zebrafish models [74]. This evidence concerns the gene DHCR7-DT and age-related macular degeneration.