locus will yield other risk alleles of smaller effect. Although such dissection is proving to be a tough task, there are already examples of success. After the identification of a risk allele for macular degeneration, a polymorphism that causes the substitution of tyrosine for histidine at position 402 in complement factor H (CFH),41–43 several additional and independent risk variants, including noncoding alterations, have been detected in and around the CFH gene, and none of these variants in isolation account for all the risk attributed to this locus.44
