The emotional component of incentive salience is evaluated and modulated by pgACC and OFC. pgACC is shown to be involved in a top-down frontostriatal gating system that prevents erroneous or irrelevant sensory stimuli from reaching the cortex28. Dysfunction in this system has been shown to lead to various disorders such as tinnitus, chronic pain, etc.29. The pgACC has also been implicated to reduce aggression by exercising control over the amygdala and thus acts as a disorder-general suppression system30. pgACC and OFC are also proposed to evaluate the pleasure of salient stimuli and to prioritize behaviorally relevant stimuli31. The OFC itself has been shown to be involved in the assignment of reward and reward-based decision making along with the NAcc, VS, VTA, and the amygdala32,33. Thus, the pathological increase in both BOLD signal and beta activity in pgACC may be characteristic of dysfunctional suppression of craving. This may be confirmed with the results of our previous studies, which reported a reduction in this abnormal pgACC activity following rTMS targeting the dACC, leading to suppression of craving7. Additionally, hyperactivation in pgACC among
