JAK2 and acquired polycythemia vera: The hematologic and splenic phenotype of this model, and the degree of upregulation of erythroferrone, was consistent with human PV disease although less severe than previous knockin models of Jak2-V617F PV, which have exhibited a stronger phenotype, with higher hemoglobin and hematocrit levels and greater degrees of splenomegaly22,39,66,67; these models may exhibit more marked elevations in erythroferrone, and deletion of erythroferrone in these models may induce a change in hepcidin levels and changes in systemic iron physiology.