George R. Breese, PhD, was a longtime faculty at the University of North Carolina School of Medicine and the Bowles Center for Alcohol Studies. Dr. Breese passed away in late June following several years of poor health. Dr. Breese earned his Bachelor’s in Pharmacy from Butler University in 1959, a Master’s in Pharmacology from Butler University in 1961, and a PhD in Pharmacology from the University of Tennessee in 1965. He had additional training at the University of Arkansas Medical School and as an NIH fellow with Dr. Irwin Kopin from 1966-68. He joined the UNC faculty in 1968 as an Assistant Professor of Psychiatry and Pharmacology at the Brain Development Research Center. He was an ACNP Member Emeritus, having been accepted in 1973. At UNC he became a Full Professor in 1977. He joined the Bowles Center for Alcohol Studies in 1995 and was named a John Andrews Distinguished Professor in 2008. He retired from UNC in 2020. For much of his career, he studied the mechanisms of drug-induced changes in behavior, particularly antidepressants, stimulants, and alcohol. Early in his career, he focused on brain dopamine (DA), norepinephrine, and serotonin. He was among the first to study 6-hydroxy-dopamine, (6-OH-DA) and determined it was a selective dopamine neuron toxin [1]; this became a popular method contributing to studies on addiction and Parkinson’s disease. Using 6-OH-DA in neonatal rats, he developed a model of Lesch-Nyham syndrome [2]. Later in his career, he discovered multiple withdrawals from alcohol “kindled” inferior collicular seizures [3], which led to seminal studies related to multiple alcohol withdrawals from moderate ethanol exposure leading to increased increasing anxiety [4]. This finding has emerged as highly relevant to understanding the human experience and alcohol use disorders (AUD). His mechanistic studies uncovered changes in GABA receptors, in corticotropin-release factor (CRF), and in brain proinflammatory cytokines within the central amygdala that continue to be investigated broadly in studies on AUD [5]. His discovery that multiple ethanol exposures cause progressive increases in anxiety continues to provide potential druggable targets for the treatment of AUD. He trained countless scientists in his lab, many of whom continue to have productive careers. His passion for science was remarkable. He was always ready to talk about science and how to push ideas forward for better AUD treatments. He will be missed, but his work will continue to inspire us all.