ICAM1 and Venous thrombosis: Similarly, ECs of the spleen and splenic vein were described to be JAK2-mutated [93], and Edelmann et al. demonstrated in a JAK2V617F mouse model that β1 and β2 integrins of JAK2V617F-positive granulocytes revealed higher affinity than their normal counterparts to vascular cell adhesion molecule 1 (VCAM1) and intercellular adhesion molecule 1 (ICAM1), promoting venous thrombosis [94].