We have identified a number of candidate causal genes for DPW and AUD, resulting from a multi-omic analysis of human genetic and expression data. Our resource in conjunction with data generated in animal studies will guide researchers to plan well-informed experiments. The current study also has some limitations. We want to emphasize that due to the limited availability of raw GWAS and e/mQTL data we were not able to perform sex-stratified analyses. There was also no data on alcohol consumption/ alcohol dependence in individuals contributing to the myeloid datasets. This limited us in comparisons of predicted gene expression changes (SMR analyses) in the myeloid cells to actual gene expression changes in monocytes or other myeloid cells. The differential expression results from the brains of people with alcohol use were also generated in a small dataset (Total N = 138; NAlc Con = 92) (although this represents the largest dataset to date). Given the smaller effect sizes of GWAS signals it will require a very large brain dataset to detect associations of SNP mediated mRNA expression with phenotype. Still our data validated key genes at nominal association levels, which are encouraging for further targeted studies.
