These molecular abnormalities result in a constitutive activation of the JAK/signal transducer and activator of transcription (STAT) signaling pathway and contribute to cytokine hypersensitivity and cytokine independent growth of the mutant cells, as exemplified by the erythropoietin-independent erythroid colonies (EEC) typically found in most PV patients [9], [10]. This evidence concerns the gene EPO and acquired polycythemia vera.