Burns proposes an intriguing hypothesis by suggesting that the “schizophrenia genes” might not be regulatory genes themselves, but rather closely associated with regulatory genes directly involved in the proper growth of the social brain. We point out that this account would benefit from incorporating the effects of localized lesions and aberrant hemispheric asymmetry on cortical connectivity underlying the social brain. In addition, we argue that the evolutionary framework is superfluous.

We argue that the pivotal role assigned by Northoff to the principle of top-down modulation in catatonia might successfully be applied to other symptoms of schizophrenia, for example, hallucinations. Second, we propose that Northoff's account would benefit from a more comprehensive analysis of the cognitive level of explanation. Finally, contrary to Northoff, we hypothesize that “top-down modulation” might play as important a role as “horizontal modulation” in affective-behavioral alterations.

Although the evidence remains tentative at best, the conception of hallucinations in schizophrenia as being underconstrained perception resulting from intrinsic thalamocortical resonance in sensory areas might complement current models of hallucination. However, in itself, the approach falls short of comprehensively explaining the neurogenesis of hallucinations in schizophrenia, as it neglects the role of external attributional biases, mental imagery, and a disconnection between frontal and temporal areas.

In this commentary we argue that evolution of the human brain to host the language system was accomplished by the selective development of frontal and temporal areas in the left hemisphere. The unilateral development of Broca's and Wernicke's areas could have resulted from one or more transcription factors that have an expression pattern restricted to the left hemisphere.