Dysregulation of the JAK/STAT pathway, resulting from the occurrence of one of the three so called “driver mutations”, i.e., JAK2 exon 14 and exon 12 mutations, thrombopoietin receptor gene (Myeloproliferative Leukemia Protein, MPL) mutations or calreticulin (CALR) mutations, has been traditionally identified as the link between the neoplastic clone and cytokine overproduction in MF (and MPN in general) [7]. The gene discussed is SOAT1; the disease is myeloproliferative neoplasm.