We published a comprehensive review of the genetics of alcoholism over a decade ago [1]. Since then, there have been significant advances in techniques available for mapping genes and as a result considerable changes in outlook have occurred. It is now generally accepted that genetic risk for alcoholism is likely to be due to common variants in numerous genes, each of small effect, however rare variants with large effects might also play a role. After years of family-based linkage studies and case-control candidate gene studies, attention has shifted to large scale genome-wide association studies (GWAS) for the detection of novel common variants (≥ 1%). Exome and whole genome sequencing studies for the detection of rare variants are beginning to emerge. Moreover, it is increasingly recognized that childhood trauma, particularly in the first few years of life, is a strong predictor 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
