Introduction: Prenatal exposure to excess androgens, as environmental factors affecting the fetal epigenome, and also a potent agent for developing special phenotypes in adulthood, has been the subject of many studies during recent decades. Results of various molecular studies conducted in this area indicate that exposure to androgens, during certain periods of growth and development of the fetus, affects cellular processes, tissues and organ development leading to phenotype and behavior alterations, one of which is causing susceptibility to polycystic ovary syndrome in adulthood. Testosterone, the most important androgen, has interfering effects in metabolic and endocrine pathways, usually a result of epigenetic changes. In recognition of diverted pathways leading to the development of disease conditions and considering possible interventions at the molecular level in these directions, control of prenatal environment and conditions can be taken to account as the first and most important step in prevention of related diseases. This article reviews the studies on the epigenetic and gene expression changes of various biological pathways as a result of this exposure, using the polycystic ovarian syndrome as an appropriate model to illustrate this exposure.