their efficacy remain unclear. A key question for future studies is whether these treatments target the brain, the peripheral immune system, or a combination of both to exert their behavioral effects. Studies utilizing global KO mice demonstrate numerous cytokines and chemokines can regulate alcohol drinking, but since neuroimmune molecules are normally expressed in a variety of tissues and cell types, pinpointing the behaviorally relevant functional context is difficult. Microglia and astrocyte dysregulation are hallmarks of chronic alcohol exposure, but their individual and collective contributions to neuroimmune-mediated behaviors are relatively unknown. Furthermore, most studies targeting astrocytes or microglia do not account for glial heterogeneity within and across brain regions or pathological states. Single cell sequencing approaches to identify more specific molecular indicators of addiction-associated microglia and astrocytes may be useful to address this issue (Keren-Shaul et al., 2017). Future research will also need to examine unique stages, time courses, and neuronal consequences of glial activation during the development and progression of AUD. These questions are in the early stages of investigation and are key to dissecting neuroimmune signaling in alcohol-related behaviors and developing targeted treatments. Newer tools, including cell-type specific depletion drugs (Walter and Crews, 2017), brain-region specific viral manipulations (Scofield
