Anaphylaxis is a systemic, life-threatening allergic reaction that can affect various organs in a short time. The most common cause include food, insect toxins, drugs, and latex. The disease results from degranulation of the main effector cells of anaphylaxis, i.e. mast cells and basophils. Upon contact with the appropriate allergen, effector cells release inflammatory immune mediators such as tryptase, histamine, and serotonin. These mediators cause various clinical signs such as increased vascular permeability, soft tissue swelling, hypotension, itching, nausea, etc. According to clinical signs, anaphylaxis can be divided into four classes, according to Mueller's classification. The genetic background is thought to have a big impact on the occurrence of anaphylaxis, but the gene or genes responsible for this are not yet known. The study analyzed whether the rs1024611 polymorphism in the CCL2 gene influences the development and severity of anaphylaxis. DNA was isolated from the blood of 1462 patients with diagnosed hypersensitivity to Hymenoptera venom, with different reaction severities s and 201 healthy individuals, and then the genotype of the rs1024611 polymorphism was determined by real-time PCR. The study results did not support the hypothesis that the polymorphism in the CCL2 gene affects the reaction severity and that, consequently, people with a certain genotype are more susceptible to anaphylaxis. We observed a trend that the GG genotype of the rs1024611 polymorphism in the CCL2 gene affects a higher basal serum concentration of the chemokine CCL2, but due to the small number of individuals with this genotype and measured basal concentration of the chemokine CCL2 is not statistically significant.