for the development of later psychopathology, including alcoholism, and some of the genetic risk may only become apparent in the context of childhood trauma (i.e. gene x environment (G x E) interactions). However, it should be borne in mind that no matter how sophisticated genetic techniques might become, further advances in detecting genotype – phenotype associations are hampered by the fact that alcoholism is a heterogeneous phenotype. One way around this has been the use of intermediate phenotypes, including electrophysiological and imaging, that reflect mediating factors in behavior and are likely to be influenced by variation at fewer genes. Another approach is to refine the phenotype. In recent years there have been attempts at empirical classification of alcoholics into clinically relevant and potentially genetically distinct subgroups based on the large National Epidemiologic Survey on Alcohol and Related Conditions (NESARC) [2] that will be discussed later. Finally, the diagnostic criteria for the alcoholism phenotype (now called alcohol use disorder (AUD)) have just been radically revised in the Diagnostic and Statistical Manual of Mental Disorders, Fifth Edition (DSM-5) [3]. The aim of this review is to highlight some recent studies in human research that are of particular interest and not to provide
