A number of alterations, such as excess cytokines and increased JAK1 signaling, as well mutations in JAK2 and mutations involving the thrombopoietin receptor (TPO-r or myeloproliferative leukemia, MPL, oncogene) have also been implicated in the etiology and symptomatology of MF, PV, and ET [33-36]. The gene discussed is MPL; the disease is acquired polycythemia vera.