Given the large literature on the involvement of heightened noradrenergic signaling, particularly in the amygdala, for both stress- and alcohol-related behaviors, including the potential clinical use of α2AAR agonists as a treatment for alcohol use disorders [33,34,35], GRK2-mediated phosphorylation of α2AAR after adolescent CORT exposure is a strong candidate as a mediator of increased motivation for alcohol. This evidence concerns the gene CORT and alcohol abuse.