The observed increase in thrombin levels in SVT MPN+ patients is possibly driven by the increased activation of platelets and leukocytes, release of procoagulant microparticles, or endothelial dysfunction associated with JAK2 V617F: This mutation has been shown to induce the expression of P-selectin on endothelial cells, which facilitates interactions between platelets, leukocytes, and the vessel wall and, thereby, increases thrombin generation [37,38]. This evidence concerns the gene SELP and myeloproliferative disorder.