neuronal subtypes can be utilized for functional readouts, thus offering a novel platform for modeling the genetic (or epigenetic) contribution to familial or sporadic AUDs (Soliman et al., 2017). Alcohol abuse contributes to mortality and cancer development, on a global scale. AUDs are extremely complex and composed of both pathophysiological and etiological effects, and might often intertwine, which makes accuracy and precision in disease modeling essential. A clear elucidation of the molecular and cellular mechanisms specific to a subject with an AUD potentially will provide effective interventions for their clinical manifestations, or maybe preventions of the morbidity. Human stem cell technology allows pivotal biological questions to be asked in a human neuronal context. For example, how does a genetic variant that predisposes an individual to develop an AUD fit into a certain molecular pathway(s)? AUDs like all neuropsychiatric disorders, often impact many brain regions and cellular subtypes, which are often difficult to study especially in an in vitro model system. However, recent advances in 3D organoid models (Dutta, Heo, & Clevers, 2017), as well as grafting human neuronal or glial tissue into mouse brains and then follow their behavioral modifications (Han et al., 2013), potentially will offer new insights into
