As opposed to SE in acute anemic states, which is a polyclonal and EPO-dependent physiological, transient, and adaptive compensatory response, chronic SE in PV is a maladaptive, clonal process driven by mutations in JAK2 leading to autonomous, cytokine-independent erythroid proliferation, despite normal or low erythropoietin (EPO) levels [7,8,9]. The gene discussed is JAK2; the disease is acquired polycythemia vera.