In breast cancer cells, cell-to-cell interaction between vascular cell adhesion molecule 1-positive bone-tropic cells and very late antigen 4-positive osteoclast precursors activate the survival signal through the PI3K/AKT pathway; osteoclast precursors differentiate into osteoclasts through the receptor activator of NF-κB ligand (RANKL)-RANK signaling to promote osteolysis. This evidence concerns the gene AKT1 and breast cancer.