One might expect the drug resistance to JAK2 inhibitors by acquisition of mutations in the ATP-binding pocket of the TK domain of JAK2 and/or via the amplification of JAK2. We can also expect that JAK2 inhibitors are efficient to alleviate the clinical symptoms of patients with MPN, when used as monotherapy, but inefficient to cure the disease as happened with imatinib [40]. The gene discussed is JAK2; the disease is myeloproliferative disorder.