SOAT1 and myeloproliferative neoplasm: The MPLS204P is a weak gain-of-function mutation that induces constitutive STAT activation and more prolonged ligand-induced STAT phosphorylation than wild-type MPL, while MPLY591N is associated with MPLW515A and in a mouse model induced a more aggressive MPN behavior than that associated with a single MPLY591N mutant (87).