Activating mutations in Janus kinase 2 (JAK2)-, the thrombopoietin receptor- or the Calreticulin-gene cause constitutive activation of the JAK-STAT pathway and are oncogenic drivers of classic myeloproliferative neoplasms (MPN), like Polycythemia vera (PV), Essential thrombocythemia (ET) and Myelofibrosis (MF) [1, 2]. This evidence concerns the gene SOAT1 and myeloproliferative neoplasm.