Abnormal JAK2V617F-mediated Rap1-GTPase activation in neuthrophils, resulting in increased VCAM1/ICAM1-mediated cell adhesion to the endothelium108 and neutrophil extracellular trap formation109, may mechanistically link mutated JAK2 to thrombosis pathogenesis. The gene discussed is ICAM1; the disease is deep vein thrombosis.