Myelofibrosis (MF) is a rare chronic myeloproliferative neoplasm (MPN) that appears de novo (primary myelofibrosis [PMF]), or after previous polycythemia vera (PV) or essential thrombocythemia (ET) (secondary myelofibrosis [SMF]).1 Constitutive signaling through the JAK-STAT pathway via activating mutations of JAK2, CALR, and MPL genes plays a key role in its pathogenesis, while concomitant somatic mutations, mostly affecting epigenetic modifiers or spliceosome components, may influence clinical phenotype or promote disease progression.2,3. This evidence concerns the gene SOAT1 and myeloproliferative neoplasm.