Schizophrenia (SZ) is a pervasive neurodevelopmental disorder entailing social and cognitive deficits, including marked problems with language. SZ incidence has always been high and quite stable in human populations, across time and regardless of cultural implications, due to unclear reasons. Also, its complex multifactorial aetiopathogenesis, including genetic and environmental factors, is widely uncertain. It has been hypothesised that SZ pathophysiology may involve the biological components that changed during the recent human evolutionary history and led to our distinctive mode of cognition, which includes language skills. In this paper we explore this possibility, focusing on the self-domestication of the human species. This has been claimed to account for many human-specific distinctive traits, including aspects of our linguistic abilities. The domestication syndrome in mammals comprises the constellation of traits exhibited by domesticated strains, seemingly resulting from the hypofunction of the neural crest. It is our intention to show that people with SZ exhibit more marked domesticated traits at the morphological, physiological, and behavioural levels. We also show that many SZ candidate genes are found among the genes involved in the domestication syndrome, but also among genes implicated in language evolution. Finally, we show that selected genes important for the neural crest development exhibit altered expression profiles in the brain of SZ patients, specifically in areas involved in language processing. Based on these observations, we conclude that language dysfunction in SZ may represent an abnormal ontogenetic itinerary for the human faculty of language, resulting, at least in part, from changes in genes important for the domestication syndrome and, primarily involving the neural crest.