GABA-BRs mediate the slow and prolonged phase of synaptic inhibition,54 and have been implicated in the rewarding effects of drugs of abuse.55 GABA-B agonists decrease alcohol consumption and craving in humans and severity of alcohol-withdrawal symptoms in humans and rats.56 Consistent with this, GABA-BR1 expression is decreased in the hippocampus of alcoholics.55 Our findings of alcohol-dose-associated shift in JAKMIP1 TV expression implicate it as an additional mechanism that may modulate GABAB signaling, by regulating the translation and trafficking of GABA-BR to the cell surface. The gene discussed is JAKMIP1; the disease is alcohol dependence.