Philadelphia chromosome–negative myeloproliferative neoplasms (MPNs), including myelofibrosis (MF), polycythemia vera (PV), and essential thrombocythemia (ET), are genetically related, but heterogeneous chronic diseases characterized by overactive signaling through the Janus kinase (JAK)-signal transducer and activator of transcription (STAT) pathway as the central pathogenic mechanism [1–5]. The gene discussed is SOAT1; the disease is acquired polycythemia vera.