In summary, our data suggest that a proinflammatory state is created in the leukemic BMM in B-ALL by the release of Tnfα, which leads to remodeling of the BMM, breakdown of the ECM, and increased invasion of leukemia cells via the secretion of MMP-9 from MSC. The gene discussed is TNF; the disease is precursor B-cell acute lymphoblastic leukemia.