Cacioppo et al 1 make the important point that the study of normal and abnormal social behavior is essential in the understanding of mental disorders. Indeed, it is hard to imagine a mental disorder that does not involve, or lead to, abnormalities in social interaction. One could even say that one of the hallmarks of mental illness is that social interactions are affected. Obviously, and as argued by many, the human species is a social species and therefore its brain is developed to support social activities. The paper provides three examples of psychiatric disorders where abnormalities in social functioning are involved: major depressive disorder, antisocial personality and hypoactive sexual desire disorder. However, the relationship between abnormal social activities and these three disorders may be quite dissimilar. One could argue that in major depression the abnormalities in social interactions are secondary to the disease and may therefore be important in treatment and rehabilitation but not as important in understanding the etiology of the illness 2. In contrast, antisocial personality disorder is characterized at its core by abnormal social interaction, where the abnormality may be lifelong and of a developmental nature. Finally, hypoactive sexual desire disorder may lead to social interaction abnormalities, but these may not be the cause of the illness. The authors mention, but do not address in detail, two other mental disorders where abnormal social interaction, specifically impaired social cognition, may be a root cause of the illness: autism 3 and schizophrenia 4. Emotional and cognitive dysfunctions are the core clinical features of schizophrenia 5. Moreover, it has been argued that impairments in emotion recognition and theory of mind (ToM) may even trump the value of general cognition and symptoms in explaining outcome in schizophrenia 6. In healthy individuals, social cognition has been extensively studied using functional and structural imaging, and a network of brain regions subserving it has been identified 7. In short, the processing of facial expressions depends critically on the amygdala and the orbitofrontal cortex, whereas in mentalizing tasks, such as ToM, the medial and orbitofrontal cortex is critical 8. In schizophrenia, functional neuroimaging studies have consistently demonstrated reduced activity of the amygdala during processing of facial emotions compared to healthy controls 9, and reduced activation of the prefrontal cortex (PFC) has been related to impaired performance on ToM tasks. Indeed, a recent meta-analysis of functional imaging studies, comprising 450 schizophrenia patients and 422 healthy controls, has shown reduced amygdala and PFC activity in social cognition in schizophrenia 10. In contrast to the numerous functional neuroimaging studies in schizophrenia, only few structural imaging studies have investigated the relationship between abnormalities of the amygdala and PFC and social cognitive deficits seen in patients. So far, samples have been small (between 16 and 38 patients), and the influence of IQ and symptomatology has often been disregarded. We recently completed a study where we investigated whether social cognitive deficits in patients with schizophrenia are related to gray matter volume abnormalities of the amygdala and PFC. We assessed facial emotion recognition and ToM in 166 patients with schizophrenia and 134 healthy controls, and magnetic resonance imaging brain scans were acquired. Preliminary results suggest that reduced PFC, but not amygdala, gray matter volume is associated with social cognitive deficits in schizophrenia 11. Thus, anatomical abnormalities in schizophrenia may in part be related to social cognitive dysfunction. Whether this is specific to schizophrenia or these anatomical changes are also observed in other disorders characterized by social deficits remains to be studied. All in all, Cacioppo et al's paper makes a very important and compelling case that social neuroscience should be integrated into psychiatry and may make important contributions in understanding the etiology and sequelae of mental disorders. However, there is a lot of pioneering work that needs to be done to start understanding the role of this important human aspect in the etiology and course of psychiatric illness.