For example, while various mesenchymal stromal cell (MSC) subsets have been studied, including Nestin+ (10), Gli1+ (11) and Leptin-receptor+ MSCs (12), little is known about the subtypes and transcriptional states of bone marrow fibroblasts in myelofibrosis, and the specific cellular mediators and receptor-ligand (R-L) interactions that lead to pathological stromal cell activation. The gene discussed is LEPR; the disease is myelofibrosis.