not yet been applied to AD, a recent study on height (Yang et al., 2011a) indicated that if all the SNPs on a particular genotyping platform are considered simultaneously, approximately 45% of the variation in height can be captured. Consequently, the modeling of cumulative variant/gene effects and the capture of rare causal variants are crucial to the examination of complex traits. Unlike gene-set and whole genome prediction, pathway enrichment approaches capitalize on the wealth of data stored in bioinformatics databases, such as the Gene Ontology database (Ashburner et al., 2000), the Mouse Genome Informatics database (Blake et al., 2011), the Kyoto Encyclopedia of Genes and Genomes (Kanehisa, 2002), the Human Protein Reference Database (Mishra et al., 2006), HumanCyc (Romero et al., 2005), and Panther Pathways (Mi and Thomas, 2009). For example, a recent GWAS by Kendler et al. (2011) used ALIGATOR (Holmans et al., 2009), a method useful for testing the overrepresentation of Gene Ontology terms in gene lists identified from a GWAS study, to examine the genetic etiology of AD in the Molecular Genetics of Schizophrenia Control Sample. Although no SNPs survived multiple testing corrections, Kendler et al. identified six genes in the European American sample and five genes
