Background: Background:The clinical course of myeloproliferative neoplasms (MPN) is often complicated by impaired microcirculation, arterial and venous thrombosis. According to the literature, common for MPNs JAK2 gene mutations may contribute to the development of venous thrombosis. Even in the absence of overt MPN, a significant proportion of patients with recurrent cerebral and/or portal vein thrombosis carry the JAK2 V617F mutation. It is known that hereditary thrombophilic conditions, such as congenital deficiency of anticoagulants (antithrombin, protein C, and protein S) and genetic mutations (factor V Leiden, prothrombin G20210A, etc.), play an important role in the pathogenesis of venous thrombosis. However, limited data concerning the potential contribution of these mutations to the thrombotic risk in MPNs have been provided so far.