Different pathogenic models were proposed, where MPN-associated inflammation could be either the consequence of the JAK2V617F mutation in the MPN clone (i.e. “clonal inflammation”), or an early event predisposing patients to the acquisition of JAK/STAT-activating mutations in myeloid progenitors and the development of MPN (10–13, 31, 32). This evidence concerns the gene SOAT1 and myeloproliferative disorder.