The fairly widespread prevalence of CRSwNP along with the lack of remedies for curing the disease, a variety of hypotheses of etiology dictate the need for further study of all links in the pathogenesis and clinical features of the course of the disease. In the coming century of “biological medicine”, the availability of high technologies of medical genetics makes it possible to reveal the individual characteristics of the most important regulatory systems of the body, which opens up new prospects for studying the etiology and pathogenesis of CRSwNP. In the tissues of polyps and intranasal secretions, an increase in the concentration of various inflammatory mediators, in particular interleukins, is observed due to an increase in their de novo synthesis by effector cells. Particular importance is attached to an increase in the concentration of cytokines involved in the development, recruitment and activation of eosinophils (IL-4, IL-12, IL-13, GM-CSF), the main pro-inflammatory (IL-1, IL-2, TNF-a, IL- 10), regulatory cytokines (IL-10, TLR2B), contributing to the chronicity of the inflammatory process in the nasal cavity.