As regards the endosteal niche, in a murine model of MPN, Schepers et al. demonstrated an abnormal osteoblast expansion due to overstimulation by MSCs, associated with the overproduction of inflammatory cytokines, the promotion of fibrogenesis and the downregulation of CXCL12 expression (which is essential for the maintenance of quiescent HSCs and controlled HSC mobilization), leading to the establishment of a “self-reinforcing” MPN niche [79]. This evidence concerns the gene CXCL12 and myeloproliferative disorder.