Second, it has also been reported in mouse models of Chuvash polycythemia that abnormal erythrocytosis results not only from HIF upregulation, but also from VHL‐dependent, HIF‐independent activation of the JAK‐STAT signaling pathway, leading to enhanced sensitivity of erythroid precursor cells to erythropoietin (Russell et al. The gene discussed is SOAT1; the disease is Chuvash polycythemia.