Ono et al. established such a model, and after co-culturing mouse bone marrow-infiltrated breast cancer (BM2) cells with human bone marrow mesenchymal stem cells (BM-MSCs), they found that expression of myristoylated alanine-rich C-kinase substrate(MARCKS), a target gene of miR-23b that is related to cell invasion and cell cycling, was significantly reduced in BM2 cells via transfer of BM-MSC-derived exosomal miR-23b. The gene discussed is MARCKS; the disease is breast cancer.