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. The gene discussed is SOAT1; the disease is essential thrombocythemia.