Myelofibrosis (MF) is a chronic myeloproliferative neoplasm (MPN) characterized by clonal proliferation of hematopoietic progenitors, bone marrow fibrosis, and extramedullary hematopoiesis. Constitutive activation of JAK-STAT pathway signaling through mutations in the MPN driver genes (i.e., JAK2, CALR, and MPL) plays a fundamental role in its pathogenesis and progression, which can be influenced by mutations in other genes (non-MPN driver genes) [1].

Thrombotic complications increase morbidity and mortality in MF [2,3,4,5]. Around 20% of patients experience thrombosis before or at diagnosis, with 6–12% developing thrombotic events during follow-up. The main risk factors for thrombosis include older age, a prior history of thrombosis, and a JAK2 mutated genotype [2, 3]. While several studies have evaluated non-MPN driver gene mutations as risk factors for thrombosis in essential thrombocythemia (ET) [6, 7] and polycythemia vera (PV) [8, 9], their role in MF is less defined.

骨髓纤维化 （MF） 是一种慢性骨髓增生性肿瘤 （MPN），其特征是造血祖细胞克隆性增殖、骨髓纤维化和髓外造血。通过 MPN 驱动基因（即 JAK2、CALR 和 MPL）突变对 JAK-STAT 通路信号传导进行组成型激活，在其发病机制和进展中起着重要作用，这可能受到其他基因（非 MPN 驱动基因）突变的影响 [1]。

血栓形成并发症会增加 MF 的并发症发生率和死亡率 [2,3,4,5]。大约 20% 的患者在诊断前或诊断时出现血栓形成，其中 6-12% 的患者在随访期间发生血栓形成事件。血栓形成的主要危险因素包括高龄、血栓形成既往史和 JAK2 突变基因型 [2， 3]。虽然有几项研究评估了非 MPN 驱动基因突变是原发性血小板增多症 （ET） [6， 7] 和真性红细胞增多症 （PV） [8， 9] 中血栓形成的危险因素，但它们在 MF 中的作用尚不清楚。