In recent years, the prevalence of autoimmune thyroid diseases, particularly autoimmune thyroiditis and Graves’ disease, has increased. These conditions sometimes co‑occur as part of an autoimmune ‘overlap’ syndrome. Among the triggers of this lesion, both genetic factors and environmental factors are considered, which under certain conditions contribute to the realization of manifestations of the autoimmune continuum, which can occur either simultaneously or sequentially. Despite the presence of a number of scientific studies, the issues of pathogenesis and clinical course of autoimmune «overlap» syndrome remain still not fully clarified. Objective — to analyze possible triggers of autoimmune «overlap» syndrome and to clarify the features of the clinical course of thyroid diseases using the example of a clinical case. A case from real clinical practice of a patient with autoimmune overlap syndrome is considered. Patient O., 33 years old, works as a manicurist. She complained of palpitations, shortness of breath with light exertion, insomnia, some imbalance, weight loss, fatigue. History of unsuccessful in vitro fertilization; first pregnancy with a frozen fetus at 8 weeks, which was observed in the rudimentary horn of the uterus; second pregnancy, which ended in spontaneous miscarriage at 17—18 weeks. After that, 3 months later, the first manifestation of Graves’ disease occurred, thyreostatic treatment with thiamazole was prescribed for 2.5 months, discontinued due to an allergic reaction, and euthyroidism was achieved. However, a slight increase in antibodies to rTSH was observed against the background of a significant increase in the production of AT‑TPO and AT‑TG. Structural changes in the thyroid gland, characteristic of autoimmune thyroiditis, were also noted. Spontaneous improvement of the condition contributed to the third pregnancy, and the patient gave birth to a healthy boy. She breastfed for 1.2 years, but a year after giving birth, a relapse occurred. Clinical symptoms consistent with diffuse toxic goiter were detected, a decrease in vitamin D levels along with moderate thyroid hyperplasia. She was treated with carbomazole until hormonal balance was achieved and antibodies to rTSH decreased, unfortunately only for 8 months. Almost a year later, a relapse occurred again. It is known that her sister also has thyroid disease. On examination: exophthalmos and ocular symptoms of thyrotoxicosis are absent, tremor of the upper extremities is present. Heart activity is rhythmic, tones are of normal volume, soft systolic murmur at the apex, tachycardia up to 110—120 /min, blood pressure 100/70 mm Hg. A decrease in TSH to 0.285 mU/mL, an increase in vT4 to 2.17 ng/dL, in T3—3.28 pg/mL, as well as an increase in the production of AT‑rTSH, AT‑TPO, AT‑TG, mild anemia. Ultrasound shows slight hyperplasia of the thyroid gland, focally increased echogenicity, the structure is heterogeneous, mosaic, hypervascularization. Considering the existing clinical symptoms of thyrotoxicosis with characteristic changes in the thyroid gland, inherent in both diseases, a diagnosis of autoimmune «overlap» syndrome was made. The patient was treated conservatively with the appointment of carbimazole, B‑complex vitamins, Sorbifer, Anaprilin until the onset of clinical and immunological remission and inhibition of autoaggression processes. Conclusions. The primary triggers of autoimmune ‘overlap’ syndrome include genetic predisposition, especially in young women, along with stress, vitamin D deficiency, exposure to certain chemicals (including acetone‑containing substances), and the use of hormonal medications, particularly progesterone. Autoimmune Overlap syndrome should be considered as a syndrome that combines two thyroid diseases, and the clinical course may be with the initial manifestation of Graves’ disease, and later — the addition of autoimmune thyroiditis with a recurrent course, which requires careful study to develop a personalized rational treatment, giving preference to conservative. The presence of autoimmune «overlap» syndrome contributes to the peculiarities of the clinical manifestations of thyroid diseases, in particular, Graves’ disease is manifested by thyrotoxic cardiomyopathy, neuropathy with moderate hyperplasia and heterogeneity of the thyroid gland structure against the background of a significant increase in autoaggression in the absence of thyrotoxic ophthalmopathy and dermopathy.