Given the methodological progressions in the previous literature, it is exciting that this study adds to the striking consistency in the reports of structural deficiencies in the temporal cortex in individuals with psychopathy. Notably, these observed structural deficiencies are mirrored in consistent reports of reduced activity within this region in functional imaging studies. Despite the robustness of these findings, it remains an open question as to how we should interpret them. They may reflect a developmental consequence of functional deficits in the amygdala, a region in which dysfunction is consistently implicated in psychopathy (6), as Ly et al. also imply. Alternatively, the results may relate to the well-documented impairment in stimulus-reinforcement learning (6) (i.e., the capacity to learn some stimuli is associated with positive outcomes and others with negative outcomes). Stimulus-reinforcement learning involves the integrated functioning of the amygdala and temporal cortex; as such, the function and structure of both these highly interconnected regions may be inevitably compromised in individuals with psychopathy. Finally, it is also possible that there may be specific computational processes, as yet unidentified, that are reliant on the temporal cortex and that are compromised in individuals with this disorder. With respect to the latter point, it should be noted that patients with autism also exhibit reduced cortical thinning within these regions of the temporal cortex (5). Autism is another disorder of social cognition, albeit one marked by computational impairments that are notably different from those in psychopathy. For example, stimulus-reinforcement learning appears to be relatively intact in autism but is severely compromised in psychopathy, while theory of mind (the capacity to include the mental states of others—their beliefs, intentions, and knowledge—in one's own internal representation of their identity) is impaired in autism but intact in psychopathy (6). It is possible that there are unidentified social cognitive functions reliant on the superior temporal cortex and temporal pole that are impaired in both disorders.