Given the universal activation of the Janus kinase (JAK) signal transducer and activator of transcription (STAT) signaling observed in the classic, Philadelphia chromosome (Ph)-negative myeloproliferative neoplasms (MPNs) [1], the central role that JAK inhibitors play in these diseases is not surprising [2,3]. The gene discussed is SOAT1; the disease is myeloproliferative disorder.