Patients with MPNs commonly experience complications caused by dysfunctional haemostasis and thrombosis. Patient treatment is limited and aimed at preventing these adverse events, typically by low-dose aspirin therapy. However, a subset of patients experience increased risk of bleeding diatheses and these patients are at an even greater risk for experiencing complications if they are treated with low-dose aspirin. Currently, there are no methods for stratifying MPN patients to distinguish those who are at risk for thrombosis or bleeding. In order to improve MPN patient treatment, a better understanding of the mechanisms behind haemostasis and thrombosis complications is required. Here, we investigate the mechanisms of JAK2V617F activation in endothelial cells and the effects of JAK2V617F on endothelial function.