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 rather than as epiphenomenon associated with the disease. In schizophrenia, multiple independent studies have implicated the major histocompatibility region (International Schizophrenia Consortium 2009; Shi et al. 2009; Stefansson et al. 2009) raising the intriguing possibility of an etiological role for an immune, autoimmune, or infectious process. In addition, some studies have highlighted the role of alternative ways in which genetic variation might be etiological, including the importance of copy number variation (Sebat et al. 2009) and even compelling empirical data that schizophrenia results from the cumulative effects of thousands of different genetic variants in an as yet unknown biological pathway (International Schizophrenia Consortium 2009).
