The 14-year latency from PV diagnosis to BCS manifestation aligns with the proposed "second hit" hypothesis, where chronic JAK/STAT activation induces endothelial dysfunction through: (i) increased circulating prothrombotic microparticles, (ii) upregulated P-selectin expression, and (iii) IL-6-mediated acute-phase response [17,20]. Notably, the patient's D-dimer elevation despite therapeutic anticoagulation suggests ongoing subclinical thrombosis, a hallmark of MPN-associated hypercoagulability. The gene discussed is SOAT1; the disease is endothelial dysfunction.