The role of constitutive activation of the JAK/STAT pathway is common across the spectrum whilst the role of co-operating mutations, epigenetic dysregulation, clonal evolution, responses to DNA damage, activation of cell signaling pathways and inflammatory activation varies resulting in differences in the observed MPN phenotype, progression of the disease and risk of thrombotic complications. The gene discussed is SOAT1; the disease is myeloproliferative neoplasm.