Indeed, TNF treatment of bone marrow organoids robustly led to a dose-dependent increase in LGALS1 expression (Fig. 7I), suggesting a model wherein a self-reinforcing, inflammatory MPN niche is created by expanded populations of basophils, mast cells, MSCs and inflammatory fibroblasts with a central role for TGFβ, TNF and galectin-1 signaling (Fig. 7J). This evidence concerns the gene TNF and myeloproliferative neoplasm.