The researchers confirmed that MSC and osteoblasts seemingly induce leukemia dormancy via osteopontin signaling, and more importantly, the system compatibility with single-cell technologies allowed the generation of a more detailed map of interactions among different types of B-ALL cells, samples and microenvironments inside the artificial BM model and how these interactions affect the sensitivity of B-ALL to chemotherapeutics [123]. The gene discussed is SPP1; the disease is precursor B-cell acute lymphoblastic leukemia.