While chronic inflammation and upregulation of the aforementioned pathways favor fibrosis, we and others have described an interferon-stimulated gene expression pattern, priming most effectively JAK2V617F-positive MPN cells for IFNa treatment in comparison to CALR-mutated cells [52,54] and highlighting important differences in inflammatory signaling and therapy response associated with the different driver oncogenes. The gene discussed is IFNA1; the disease is myeloproliferative neoplasm.