Notch deficiency in BM MSCs and endothelial cells activate the miR155/NF-κB/G-CSF/TNFα inflammation pathway to develop a myeloproliferative disease symptom such as hepatosplenomegaly, anemia, and granulocytosis (Kim et al., 2008; Wang et al., 2014); meanwhile, leukemogenic effects of fibrosis-related MSCs not only decrease hematopoietic support but also secrete pro-inflammatory s100a8/9 for HSCs-exhausted MPN and subsequent MDS initiation (Leimkuhler et al., 2021). This evidence concerns the gene NFKB1 and myeloproliferative disorder.