Objective: to study new components of the pathogenesis of ovarian dysfunction in normogonadotropic anovulation and its clinical manifestations in patients. Subjects and methods. One hundred and seventy-five patients with normogonadotropic ovarian deficiency were examined. A control group comprised healthy women with an adequate menstrual cycle (n=15). All the patients underwent conventional study, gynecological examination, small pelvic ultrasonography, and hormonal analysis by an enzyme immunoassay. Aromatase activity was estimated using the coefficient equal to the ratio of a difference between the serum levels of estradiol before and 48 hours after letrozole administration to the blood concentration of anti-Müllerian hormone, which corresponded to the number of antral follicles. Genetic examination consisted in studying the allelic variants of CYP19 (TTTA)n polymorphism, (del(TCT). Results. The lower aromatase activity of antral follicles was revealed in 40 (22.8%) patients. The majority (n=22) of the patients in this group were found to have clinical, hormonal, and echographic signs of polycystic ovary syndrome; external genital endometriosis was laparoscopically verified in 5 patients. The findings suggest that ovarian aromatase deficiency is an essential component of the pathogenesis of one of the forms of polycystic ovary syndrome. However, none of the signs of this syndrome is pathognomonic to partial ovarian aromatase deficiency, and the letrozole test is the only method for its diagnosis. Conclusion. The (TTTA)7(TTTA)11 polymorphism of the aromatase gene is significantly more common in the group of patients with normogonadotropic ovarian deficiency and a low aromatase activity in the follicles, which cannot rule out genetically determined ovarian aromatase deficiency of antral follicles in these patients. The authors declare no conflicts of interest.