The relative proportions and transcriptional activity of these cellular subsets were distinct in myelofibrosis bone marrow, with a dramatic expansion of basophils and mast cells, and relatively few eosinophils in myelofibrosis mice compared to controls (Fig. 4C), and significant enrichment of IL2-STAT5, TGFB, and TNF via NF-κB inflammatory signaling pathways (Figs. 4D and 4E). The gene discussed is IL2; the disease is myelofibrosis.