SOAT1 and acquired polycythemia vera: The constitutive activation of the JAK/STAT pathway is a pathogenetic hallmark of all MPNs, with three well‐characterised driver mutations in JAK2, CALR and MPL genes.[3, 9] JAK2V617F, a valine‐to‐phenylalanine substitution at amino acid position 617 (V617F) in exon 14 of JAK2, is the most prevalent mutation in MPNs, present in > 95% of patients with PV and in approximately 60% of patients with PMF.[3, 18] JAK2 exon 12 mutations are also observed in up to 3% of patients with PV.