It is well-known that continued inflammation may contribute to the progression of MPN.239 Thus, the activity of the JAK/STAT pathway may be elevated in response to increases in the levels of proinflammatory cytokines.243 Previous studies showed that activated STAT3 proteins could promote cytokine production in a variety of cancers.244 Using a JAK2 inhibitor to treat mice with MPN resulted in reduced cytokine levels and attenuated systemic symptoms.245 In MPNs, abnormal activation in JAK/STAT signaling is commonly accompanied by mutations in tyrosine kinases. This evidence concerns the gene SOAT1 and myeloproliferative neoplasm.