**4. Summary and conclusion**

It is generally accepted that complex diseases such as autism is influenced by genetic altera‐ tions at multiple and variable sites that interact to reach a threshold of toxicity that triggers the disease expression. When expressed chronically even small variations in the gene ex‐ pression and enzyme activity caused by genetic changes and environmental factors could have a significant impact on downstream metabolism leading to development of autism. A metabolic imbalance can promote chronic oxidative stress and impaired methylation capaci‐ ty which results in alterations of normal developmental maturation of neurologic and im‐ munologic systems associated with autism. The production of free radicals is critical in the regulation of many biological functions, cellular damage, and the pathogenesis of disorders affecting central nervous system. Oxidative stress is shown to play a role in many neuro‐ psychiatric disorders, including ASD. Understanding of functional connections of autism-as‐ sociated genes and the impact of environmental risk factors on cellular responses linked to ASD phenotype will allow to distinguish disease-related pathological as well as compensa‐ tory processes and to identify targets for treatment of different features associated with ASD. The human genetic heterogeneity increases the complexity of the effects of environ‐ mental factors. New biomarkers are desired to support clinical trials which are the final way to find out the efficiency of new types of interventions.
