The primary approach to overcoming etiological heterogeneity has been the use of endophenotypes (i.e., a heritable biological and/or psychological characteristic of a disease that (1) has a strong biological basis, (2) manifests whether or not the illness is active within the individual, (3) relates to the disease in the population, and (4) co-segregates with the disease in families; Gottesman and Gould, 2003), which should improve the power to identify alcohol susceptibility genes because they reduce the complexity of both the phenotype and the genetic analysis (i.e., a less complex genetic architecture). Several of the most studied endophenotypes of AD have been electrophysiological measures, such as electroencephalography and event-related potentials (e.g., alpha and beta waves and alpha power, as well as the P300 amplitude; Carlson and Iacono, 2006; Chorlian et al., 2007), sensitivity to alcohol (i.e., level of alcohol response; Schuckit, 1994; Schuckit et al., 2004)), alcohol metabolism (Lind et al., 2008b; Martin et al., 1985a; Martin et al., 1985b), and alcohol craving (Anton, 1999; Mackillop et al., 2007, 2010; Monti et al., 2000; Sinha and O’Malley, 1999; Verheul et al.,
