With this study, Etkin and colleagues provide a research tool to measure regulation of emotional information that does not depend on self-reports and is sensitive to psychopathology. Furthermore, these findings support existing theories of emotion regulation that implicate the dorsolateral prefrontal cortex and anterior cingulate cortex (6). Most of this earlier research has used strategies that instruct study participants to modulate emotional responses (e.g., reappraisal or redirected attention) and that rely on explicit manipulations. In contrast, Etkin and colleagues examine implicit, automatic regulation. Related to this fundamental difference, previous investigations focused on experienced emotion, whereas the present study examines cognitive response (selective attention) to conflict between emotional stimuli. In other words, whereas prior work examined "emotion regulation" per se, Etkin and colleagues probe "conflict regulation" and, by using emotional stimuli, challenge neural circuits of emotion appraisal. Whether and how such automatic emotion-related responses contribute to daily emotional experiences remain unknown. However, the finding that individuals with generalized anxiety disorder are impaired on this function suggests that this deficit may contribute to affective dysregulation. In the same vein, the possibility that patients with generalized anxiety disorder could also be impaired on a purely cognitive conflict adaptation paradigm might mitigate the specific relevance of the present findings to emotion processing. Nevertheless, this would not diminish the potential treatment implications. Indeed, the "conflict adaptation" deficit might very well explain the inability of generalized anxiety disorder patients to dampen feelings of anxiety. As a result, strengthening the underlying neural network of "conflict adaptation" via relevant behavioral training could remedy this deficit (similar to the novel Attention Bias Modification Treatment developed for other anxiety disorders ).