The discovery that classicBCR-ABL1–negative myeloproliferative neoplasms (MPNs) are constantly associated with abnormal JAK2 activation due to different mutations, has paved the way for the development of JAK inhibitors in the therapy of these disorders as well as of other diseases with either genetic alterations in the JAK pathway or JAK-induced activation by autocrine and paracrine cytokine loops4,5. The gene discussed is JAK2; the disease is myeloproliferative neoplasm.