N RECENT YEARS, members of the nonprofit groupPhysicians Committee for Responsible Medicine haveregularly petitioned the National Institute on Alcohol Abuseand Alcoholism(NIAAA)AdvisoryCounciltoexclude alco-hol research in animals from their portfolio, and to insteadfocus on education and treatment in humans. Indeed, pre-vention and rehabilitation are important steps and strategiesthat are well funded by NIAAA and other groups. The pur-pose of this commentary is to argue for sustained commit-ment to basic research for effective prevention andrehabilitation of alcohol use disorders (AUDs), for whichanimals are required where there are no viable alternatives.As such, the audience for this commentary is alcoholresearchers or physicians, counselors, or anyone with aninterestinadvancingourabilitytotreatAUDs.Alcohol use has long been a dominant aspect of many cul-turesandsocietiesaroundtheworld. Whilemanyindividualsare able to consume alcohol without suffering any adverseeffects, excessive drinking and AUDs can lead to a profoundreduction in the quality of life for individuals, families, andcommunities. Consistent with an aim of NIAAA (nia-aa.nih.gov/about-niaaa), it is our responsibility to use allavailable resources to understand why and how some indi-viduals become addicted, and how to reverse or decrease thecellular pathology mediating this disease and its associatedbehaviors.An AUD currently occurs in about 18 million adults inthe United States, while excessive drinking contributes toapproximately 6% of all deaths worldwide (World HealthOrganization, 2014).Alcohol use directly contributes tomul-tipleorganpathologies(e.g.,cardiovascularandliverdisease;Djousse and Gaziano, 2008; Molina et al., 2014) in a dose-dependentfashionandisamongtheleadingcausesofprema-ture death and disability in the United States (Bauer et al.,2014). AUD is fundamentally a behavioral disease, oftenreferred to as a chronic relapsing disorder (Edwards andGross,1976).Assuch,itcanonlybemodeledbyreproducingobservable characteristics of the disease, such as excessive orimpaired control over drinking, withdrawal symptoms, andrelapse-like behavior (Leeman et al.,2014).Mostphysiologi-cal diseases originate from abnormal cellular processes thatare largely independent of volitional behavior. In contrast,AUD develops through the gradual shaping of alcoholdrinking overyearsasa causeand consequenceofchangesinthe brain, resulting in a shift in the distribution of anindivid-ual’s behavior away from more natural incentives, such asjob and family, toward a focus on obtaining and consumingalcohol. Indeed, AUD diagnoses are almost exclusivelybasedonbehaviorandpatternsofdrinkingovertime(Amer-ican Psychiatric Association, 2013). There remains an urgentneedtodevelopacomprehensiveunderstandingofthe mech-anisms driving AUD and from this to develop a variety ofclinicaltoolstocombatthisdisease.Likeotherneurobehavioraldisorders,AUD resultsfrom acomplex interplay of genetics and environment (Bell et al.,2012). How these variables alter patterns and frequency ofdrinking related to AUD is a central research emphasis atboth clinical and preclinical levels. This emphasis is crucial