Notably, a significant increase in LGALS1 was observed in patients with myelofibrosis due to either JAK2V617F or mutCALR (Fig. S6E), confirming that basophils and mast cells are likely to play an important role in the pathobiology of myelofibrosis in patients and contribute to TNF pro-inflammatory pathways. This evidence concerns the gene TNF and myelofibrosis.