Importantly, development of PV-like pathology in the JAK2V671F transgenic model was dependent on both thrombopoietin and Stat5 (signal transducer and activator of transcription 5) signaling as inactivation of either of the genes in transgenic animals abrogated manifestations of PV [68,69], Wolach et al. found that mice with knock-in of Jak2V617F have elevated risk of thrombosis due to increased propensity for neutrophil extracellular trap formation, a component of innate immunity linked to thrombosis [70]. The gene discussed is THPO; the disease is acquired polycythemia vera.