Chronic inflammation may be linked to hypoxia due to cell accumulation in the BM, which in turn was associated with JAK/STAT pathway activation by IL-6, IL-11, VEGF, HGF, PDGF, and TGF-β that mediates cell survival and proliferation, and thereby contributes to MPN pathogenesis (27, 28). This evidence concerns the gene SOAT1 and myeloproliferative neoplasm.