Reply by the current authors to the comments made by Marco Leyton & Paul Vezina (see record 2012-28726-013) on the original article (see record 2012-04725-001). The commentary by Leyton and Vezina addresses how to interpret the seemingly contradictory findings of two papers on reward processing in problem gambling (PrG). Leyton and Vezina propose that these contrasting findings could be explained by differences in specific cues used. They argue that problem gamblers show enhanced striatal activation when confronted with disorder-specific cues and attenuated responses to disorder-irrelevant appetitive stimuli. First, we propose that condition-specific striatal responses in PrG cannot be solely explained by the specific cues. Addictive behavior sensitizes dopaminergic brain mechanisms that confer incentive salience to addiction-related rewards, resulting in enhanced striatal responses when confronted with addiction cues. Several functional magnetic resonance (fMRI) studies have similarly reported increased regional brain responses, including striatal activation, to gambling cues in problem gamblers relative to controls. Second, findings of attenuated striatal responses toward natural rewards are not consistently found in PrG, as suggested by Leyton and Vezina. Studies focusing on reward processing without specific addiction-related stimuli are usually based on the dopamine reward deficiency theory. It is possible that under most conditions problem gamblers are characterized by hyporesponsive reward circuitry but that motivational attention can be successfully mobilized to enable normal or even enhanced levels of striatal activation during reward anticipation or when encountering gambling cues.