Adenomyosis is a gynecological common condition, it represents the endometrial tissue invasion in the ut myometrium. Pathophysiological, adenomyosis is associated with the process of abnormal multiplication of endometrial cells, caused, predominantly, by imbalance in sexual hormones homeostasis. The purpose of the research was to find in the scientific international literature genetic substrate of sexual hormones imbalance involved in developing of adenomyosis. The PubMed and Springer Link databases were used to identify information linked with ER-α and ER-β receptors role in adenomyosis. Adenomyosis is considered a condition dependent on the amount of estrogen in the blood and its receptors: ER-α and ERβ, which are transcription factors and modulators on the promoter level, of the expression of genes that coordinate estrogenic metabolic processes. The genetic function of these 2 receptors is antagonist-complementary: ER-β (encoded by ESR2), stimulated by estrogen, prevents cell proliferation by inhibiting the expression of the ESR1 gene, which encode the ER-α receptor, this, in the presence of high estrogen concentrations, will have a stronger and reverse action to the first: will inhibit ESR2 gene transcription, this will reduce ER-β receptor biosynthesis and will stimulate gene expression of proto oncogenes through interaction with their transcription factors. As a result, proteins synthesized by proto oncogenes will induce elevated multiplication action on specific cells. Tissue specificity of these products depend on the isoform of splicing of the mRNA gene ESR1. The dominance of the splicing variant of ESR1 is assumed to be responsible for the proliferation of endometrial cells and induction the appearance of adenomyosis. In genetic or hormonal dysfunctions, the ESR1 gene remains permanently activated and expresses continuous ER-α receptors. The stimulatory action of proto oncogenes is also induced by the membrane estrogen receptor GPER. This study shows that disorders in the expression of ERS1 and ERS2 genes can have important consequences in the appearance and development of adenomyosis. And this should be considered in aspects of ethiopathogeny.