AbstractMultiple studies demonstrating the association of aggressive behavior with allelic variants of neurotransmitter system genes appear to be controversial, while “risk” alleles have no effect on impaired gene expression and functioning of encoded proteins. To explain these associations, we suggested the role of deregulated epigenetic processes caused by the changes in the spatial configuration of transcribed proteins owing to the impaired interaction with noncoding RNAs, which results in modified functioning of genetic networks. Stressful life events occurring during the pre- and postnatal period causing changes in DNA methylation and histone modifications, which disrupt expression of neurotransmitter genes with a long-lasting effect, represent the key factors causing the manifestation of aggressive behavior. The role of stressful life events in epigenome modifications is assumed to be caused by stress-sensitive transposable elements (TEs), whose processing results in the formation of noncoding RNAs probably affecting histone modifications and methylation of certain genomic loci. Transposable elements represent the key sources of sites of binding to transcription factors and regulate genome expression, while their ability to locus-specific transpositions under the stress and self-regulation by noncoding RNAs can explain both the long-term effect of behavioral impairments and their transgenerational transfer. Prevention of behavioral impairments and phenotypic manifestations of genetic liability to aggressive behavior requires the examination of the individual nature of epigenetic modifications for the further targeted action and their correction.