These mechanisms include pro-inflammatory cytokine signaling due to aberrant Janus kinase–signal transducer and activator of transcription (JAK-STAT) pathway signaling, leading to bone marrow fibrosis and ineffective extramedullary hematopoiesis, RBC sequestration and dilution due to splenomegaly and associated increases in plasma volume, and a loss of RBCs through bleeding or destruction in circulation; dysregulated iron metabolism and non–JAK-STAT molecular alterations also contribute to dysfunctional erythropoiesis in myelofibrosis [5,6,7,8]. Here, SOAT1 is linked to myelofibrosis.