The complex genetic architecture of alcohol use and dependence results in profound clinical heterogeneity and difficulty in developing effective treatments. Animal models fail to recapitulate cellular and molecular complexities of human neurons, astrocytes, microglia, and blood brain barrier and accordingly do not capture all disease features, particularly those linked with noncoding genome sequences. Understanding precise molecular events underlying the disease and how an individual’s genetic background contributes to the disease state is essential to move into the age of personalized medicine for neuropsychiatric disorders. Despite their fairly recent development, patient derived hiPSCs have already been utilized to model a variety of psychiatric and neurodegenerative disorders. In addition to the key advantage of being human and patient specific, the ability to differentiate hiPSC into any cell type enables probing differences in cellular function and modeling of cellular interactions. In this review, we have focused on CNS cell types, but hiPSCs have also been reprogrammed into hepatocytes and adipocytes for investigation of liver function (Pashos et al., 2017; Warren et al., 2017), which is key for studying AUD. Furthermore, recent developments in
