It is presumed that its failure to reduce disease burden is not due to acquired drug resistance mutations but rather due to ruxolitinib-persistent proliferation and survival of JAK2-V617F-positive MPN cells under the condition of chronic JAK2 inhibition as well as its inhibitory effect on cytokine-activated JAK2 in normal hematopoietic cells. Here, JAK2 is linked to myeloproliferative neoplasm.