Frustration with the difficulty of treating cocaine cravings led me to an extensive review of the neuroanatomy of the ventral tegmental area, including the nucleus accumbens, which is thought to drive many aspects of addictive behaviors (1). Within the nucleus accumbens, a large number of γ-aminobutyric acid (GABA) neurons and axon fibers have been noted (2). Repeated cocaine use inhibits GABA release from nucleus accumbens axon terminals in the ventral tegmental area, where the mesolimbic dopaminergic neurons are located (3). This effect attenuates the GABA-mediated feedback inhibitory action of nucleus accumbens neurons onto ascending mesolimbic dopaminergic neurons, leading to increased activation of dopamine neurons projecting to the nucleus accumbens. Gabapentin increases brain GABA levels proportionally with dose, typically in the 800–2400-mg range (4). It was thus hypothesized that gabapentin restores the altered feedback inhibition from the nucleus accumbens. These neurobiological data, the excellent pharmacological profile of gabapentin, and a report about an addicted woman who noticed a decrease in her cravings for cocaine after she began taking 600–1500 mg/day of her husband’s gabapentin (5) prompted the trials described previously. Neither patient experienced significant side effects, such as sedation or ataxia, which are common with gabapentin therapy.