Acetylsalicylic acid (ASA) is the most common means of preventing thrombotic complications in chronic myeloproliferative neoplasms (MPNs). However, there is still no data on the role of somatic mutations in resistance to ASA therapy and there are no recommendations for considering the mutational status in the choice of the regimen of the ASA therapy for MPN. Purpose of this investigation — is investigation of mutation V617F JAK2 significance in aspirin resistance in patients with Ph-negative MPN. Material and methods. The study involved 70 patients with MPN and 12 volunteers. Platelets aggregation was performed by the impedance method in whole blood on the Chrono-Log aggregometer (USA) with ADP 5 μM and arachidonic acid 0.5 mM used as inductors. The tests were performed before and after preliminary incubation of whole blood samples in vitro with ASC 0.1 mM. or before and after incubation with a JAK inhibitor (Calbiochem). The expression of JAK2 mRNA was investigated by real-time PCR using TaqMan probes on a CFX96 («Bio-Rad») instrument. Results. In 24 out of 47 (51%) patients with MPN, a preliminary in vitro incubation of whole blood samples with ASA results in a lack of aggregation in response to induction with arachidonic acid, but there is a high response to ADP (COX-independent aspirin resistance). The inhibitor of JAK activity causes suppression of ADP-aggregation in the group of patients with high allele load V617F JAK2 (>50%), more often (p=0.01) than in the group of patients with low allele load values. It has also been shown that COX-independent aspirin resistance is associated with an increase of JAK2 mRNA level in platelets. Conclusions. The results support the hypothesis of the involvement of JAK2 in mechanisms of platelet resistance to acetylsalicylic acid.