The autism spectrum disorder (ASD) is a complex neurodevelopmental disorder with heterogeneous clinical presentation. It is characterized by deficits in the two basic domains - social (deficits of social communication and interactions) and behavioral (restrictive and repetitive patterns of behavior, interests and activities). The most important factors for development of ASD are genetic and epigenetic changes that lead to morphological-neuroanatomical, neuroimaging, and biochemical abnormalities. The most significant morphological change is an early brain overgrowth. Changes observed in neuroimaging methods are the reverse lateralization of linguistic abilities of language and speech and reduced interhemispheric connectivity. Of the biochemical abnormalities, the most pronounced is impaired serotonin neurotransmission, which negatively affects cognitive abilities and behavior. A disturbed migration of neural crest cells has been proposed by Wilkins and co-authors in 2014 as a potential explanation for the mechanism of the domestication syndrome, i.e. the phenotypic traits that a domesticated species has in comparison to its wild ancestors. The hypothesis has began to be studied and expanded also as a possible basis for autism since many features of ASD, especially those in the craniofacial area, are in direct contrast to the known features of the domestication syndrome. In this thesis, the possible interconnections between the mechanisms of human self-domestication syndrome and the development of ASD is elaborated in more detail.