Conclusion
« The knowledge of the JAK2V617F mutation in relation to PV has allowed both physicians and patients to understand that risk is not inherently based on blood counts alone but also due to the effects of JAK2V617F VAF on thrombosis and disease progression. Prospective trials are now highlighting the benefits of VAF reduction on clinical outcomes as well as certain treatment options that have a greater effect on reducing the allelic burden. However, there is still uncertainty around the degree of VAF to consistently reduce thrombotic risk, how closely peripheral VAF suppression reflects clonal suppression of JAK2-mutated cells, when to initiate therapy, and the durability of suppression after achieving reductions. These questions provide an exciting way forward to further explore superior disease-modifying therapies and better long- term clinical outcomes ».