We also investigated the underlying mechanism by which the acquired expression of CD146 in BrM-CSCs is upregulated in the specific cerebral TME and revealed a specific astrocyte-tumor intercellular regulatory axis in which astrocyte-derived growth arrest specific 6 (GAS6) induces the overexpression of CD146 in BrM-CSCs by activating its receptor AXL. The gene discussed is AXL; the disease is neoplasm.