For decades, interferon alpha (IFN‐α) has long been considered a valid treatment option in the management of classical BCR::ABL1‐negative myeloproliferative neoplasms (MPNs), which include essential thrombocythemia (ET), polycythemia vera (PV), and myelofibrosis (MF).1 The gene discussed is IFNA2; the disease is myeloproliferative disorder.