While true, MPL and CALR mutations predominantly drive ET and myelofibrosis likely due to selective expression of MPL in hematopoietic stem cells (HSCs), multipotent progenitors, common myeloid progenitors (CMPs), megakaryocyte erythroid progenitor cells (MEPs), and megakaryocyte precursor cells. Here, CALR is linked to myelofibrosis.