Genome-wide association studies (GWAS) have yielded an extraordinary and unprecedented trove of new knowledge about the genetic causes of human disease. Since 2005, well over 600 human GWAS have been published yielding genetic associations meeting stringent statistical significance (Pe'er et al. 2008) relevant to the etiology of 92 diseases and 117 other traits (Table 1) (Hindorff et al. 2009).Many of these GWAS findings have been surprising, and have engendered new ideas about disease etiology. Because exposure to genetic variation begins at the earliest stage of development, we can generally be confident that genetic risk factors are at the beginning of the causal chain that leads to disease perhaps decades later. Thus, each association is a starting point, a hard clue about disease etiology. As an example from outside of neuroscience, in Crohn's disease, GWAS implicated genes involved in macroautophagy which has provided important insights into pathogenesis (Klionsky 2009). The notably strong association of complement factor H (CFH) with age-related macular degeneration (Klein et al. 2005) has engendered renewed interest in the role of CFH role in initiating the disease process
