We reviewed the emerging clinical and biological evidence that supports the broader interpretation of arterial thrombosis as a biological turning point that identifies patients who are entering a more aggressive phase of classic myeloproliferative neoplasms. Findings from multistate analyses, international registry studies, nested case-control investigations, and recent translational research were integrated. We showed that arterial thrombosis is associated not only with recurrent vascular events but also with increased mortality, progression to myelofibrosis and blast phase, and, in selected patient populations, the subsequent development of solid cancers. We discuss the biological mechanisms that may underlie these associations, including persistent JAK2-driven inflammation, endothelial dysfunction, platelet-leukocyte interactions, neutrophil extracellular trap formation, immune remodelling, and clonal evolution. Particular attention is given to emerging biomarkers, such as JAK2V617F variant allele frequency and the neutrophil-to-lymphocyte ratio, which provide complementary information on clonal burden and inflammatory activity and may improve biological risk stratification. Finally, we discuss the clinical implications of this evolving paradigm, proposing that patients experiencing arterial thrombosis should undergo closer surveillance and be considered for biology-directed therapeutic strategies aimed at suppressing both clonal expansion and chronic thrombo-inflammation, rather than receiving secondary vascular prevention alone.
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