The objective of the study was to evaluate the frequency of the ER22/23EK and Tth111I polymorphisms in the glucocorticoid receptor gene (GR) in patients with early-onset and late-onset asthma (BA) and to assess the risk of its phenotype's development. We examined 553 BA patients and 95 apparently healthy individuals. The patients were divided into 2 groups depending on the age of BA onset: Group I included 282 patients with late-onset asthma, and group II included 271 patients with early-onset asthma. The ER22/23EK (rs 6189/6190) and Tth111I (rs10052957) polymorphisms in the GR gene were determined using polymerase chain reaction-restriction fragment length polymorphism analysis. Statistical analysis of obtained results was performed using SPSS-17 program. The analysis of frequency of genotypes and alleles for the ER22/23EK polymorphism in the GR gene with regard to the age of BA onset demonstrated a significant difference between patients with early-onset and late-onset asthma (p = 0.035). A significant difference was revealed in the distribution of alleles and genotypes for the Tth111I polymorphism in the GR gene between patients with early-onset BA and late-onset BA (p = 0.006). No correlation was found between the ER22/23EK polymorphism in the GR gene and late-onset BA in all genetic models; also, there was a reduction in the risk of early-onset BA observed in the dominant and additive models. No association was demonstrated between the Tth111I polymorphism in the GR gene and late-onset asthma, while a statistically significant correlation was shown with the risk of early-onset asthma in the dominant and super-dominant models. We established a significant difference in the distribution of alleles and genotypes for the ER22/23EK and Tth111I polymorphisms in the GR gene with regard to onset age; also, we found no association between these polymorphic variants and the development of late-onset asthma, but revealed a protective role of the ER22/23EK polymorphism in the GR gene in the dominant and additive inheritance models and of Tth111I polymorphism in the GR gene - in the dominant and super-dominant models.