We are aware of several GWAS of AD (Bierut et al., 2010; Edenberg et al., 2010; Heath et al., 2011; Johnson et al., 2006; Kendler et al., 2011; Kerner et al., 2011; Lind et al., 2010; Treutlein et al., 2009; Wang et al., 2011b, 2012; Zuo et al., 2011a, 2011b) and AD related endophenotypes, such as theta-band oscillations (Hodgkinson et al., 2010; Kang et al., 2012; Zlojutro et al., 2011), and drinking phenotypes (Baik et al., 2011; Heath et al., 2011; Pei et al., 2012; Schumann et al., 2011). These studies suggest that (1) AD is genetically heterogeneous, and (2) the complete statistical characterization of the genetic susceptibility to AD requires novel analytic techniques that can utilize all of the molecular data from both array and NGS technologies. Although a complete review is beyond the scope of this paper, we suggest recent review papers that cover GWAS of AD (Kimura and Higuchi, 2011; Treutlein and Rietschel, 2011). Notably, several GWAS have validated some candidate genes. For instance, the ADH1C gene, which has over 50 publications linking it to alcohol use/alcoholism/AD,