This is evidenced in a mouse model of BCR-ABL1+ B-ALL, where leukemic cells have been shown to reduce secretion of normal B-cell niche factors (e.g., IL-7 and CXCL12) by mesenchymal progenitors, thus contributing to the disruption of hematopoiesis and the favoring of leukemogenesis [118]. The gene discussed is CXCL12; the disease is precursor B-cell acute lymphoblastic leukemia.