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Black et al. (2026) link the observed affective switching deficits in misophonia to the role of the orbitofrontal cortex (OFC), noting that effective inhibition is essential for set-switching by suppressing competing task sets and minimizing interference during transitions. In misophonia, other works have shown the OFC shows hyperactivation specifically in response to trigger stimuli, and the authors argue this heightened activity reflects the OFC's role in facilitating functional synchronization across brain regions in ways that may directly influence behavioral task performance. From this they conclude that the reduced affective flexibility observed in misophonia is not simply a cognitive phenomenon but is grounded in identifiable neural dysregulation, with OFC hyperactivation serving as a plausible neural mechanism linking misophonic reactivity to impaired inhibitory control during affective switching (Black et al., 2026) .