An assumption was made that the increased SDF-1 secreted by TGF-β conditioned MSCs combines with the receptor CXCR4 in the TME to stimulate the activation of the SDF-1/CXCR4 signal axis, thereby promoting the interaction between MSCs with CAF-like phenotype and B-ALL cells, which promotes the migration and invasion process of B-ALL cells. This evidence concerns the gene CXCL12 and acute lymphoblastic leukemia.