The neural basis of social cognition is subject to intensive research in both humans and non-human primates. Autism is the archetypal disorder of social cognitive skills, and increasing interest is being paid to the role played by efferent and afferent connectivity between the amygdala and neocortical brain regions, in predisposing to this condition. Such circuits are now known to be critical for the processing of social information. Recent research suggests a sub-cortical neural pathway, routed through the amygdala, may turn out to be a key player in the mystery of why humans are so prone to disorders of social adjustment. This pathway responds to certain simple classes of potential threat, including direct eve contact and, in humans, arousal evoked by this exquisitely social stimulus is modulated and controlled by a variety of specific (largely frontal) neocortical regions. Dysfunction of these modulating circuits can occur in the context of developmental disorders that are associated with haploinsufficiency of one or more classes of X-linked genes, lacking Y-homologues, which may be sexually, dimorphic in expression.