The incentive sensitization theory of addiction posits that addiction is primarily caused by drug-induced sensitization in the brain's mesocorticolimbic systems, which attribute increased incentive salience to reward-associated stimuli. This hypersensitivity leads to pathological incentive motivation (wanting) for drugs. The authors address several key questions, including the role of learning in incentive sensitization, the presence of incentive sensitization in human addicts, the development of addiction-like behavior in animals, the best methods for modeling addiction symptoms in animal models, and the roles of affective pleasure and withdrawal in addiction. They argue that learning is not sufficient for pathological motivation, and that incentive sensitization is crucial for the transition to addiction. Evidence for incentive sensitization includes behavioral and neural changes in both animals and humans, such as increased attention to drug-associated cues and enhanced dopamine release in reward-related brain structures. The authors also discuss the importance of extended access procedures in animal models for producing addiction-like symptoms and the potential of experimenter-administered drugs to model addiction. Finally, they highlight the dissociation between wanting and liking in addiction, where wanting increases disproportionately to liking, and how this dissociation contributes to the persistence of addiction despite reduced pleasure.The incentive sensitization theory of addiction posits that addiction is primarily caused by drug-induced sensitization in the brain's mesocorticolimbic systems, which attribute increased incentive salience to reward-associated stimuli. This hypersensitivity leads to pathological incentive motivation (wanting) for drugs. The authors address several key questions, including the role of learning in incentive sensitization, the presence of incentive sensitization in human addicts, the development of addiction-like behavior in animals, the best methods for modeling addiction symptoms in animal models, and the roles of affective pleasure and withdrawal in addiction. They argue that learning is not sufficient for pathological motivation, and that incentive sensitization is crucial for the transition to addiction. Evidence for incentive sensitization includes behavioral and neural changes in both animals and humans, such as increased attention to drug-associated cues and enhanced dopamine release in reward-related brain structures. The authors also discuss the importance of extended access procedures in animal models for producing addiction-like symptoms and the potential of experimenter-administered drugs to model addiction. Finally, they highlight the dissociation between wanting and liking in addiction, where wanting increases disproportionately to liking, and how this dissociation contributes to the persistence of addiction despite reduced pleasure.