To the Editor: BCR::ABL1-negative chronic myeloproliferative neoplasms (MPNs), polycythemia vera (PV), essential thrombocythemia (ET), and myelofibrosis are characterized by constitutive activation of the JAK-STAT signaling pathway caused by mutations in the Janus Kinase 2 (JAK2), carelticulin, or thrombopoetin receptor genes. These neoplasms share persistent chronic inflammatory state and high cardiovascular risk. The main treatment goal in ET and PV is to prevent thrombotic events; PV patients older than >60 years or those with thrombosis history are considered to be at high risk of future thrombotic events according to European Leukemia Network (ELN) criteria, whereas prior thrombosis or age >60 years along with the presence of JAK2 mutation classifies ET patients at high risk. To mitigate thrombotic risk, all PV patients receive aspirin, as well as low-to-high ET patients. Additionally, high-risk patients are treated with hydroxyurea or interferons.1 Advanced age, leukocytosis, abnormal karyotype, and adverse mutations are associated with inferior overall survival (OS) in PV,2 while leukocytosis and prior thrombosis are the main determinants of OS in ET patients.