Glioblastoma multiforme (GBM) is a common primary tumor of the central nervous system. The change of cell stemness is one of the important characteristics of tumors including GBM, which is a cause and effect of tumor recurrence and metastasis. Previously, a large number of studies have shown that chemokines and their receptors can promote the stemness of tumor cells. Upon binging to the receptor special CXCR4, CXCL12 is involved in the proliferation, invasion and metastasis of tumor cells. Here we report the impact of CXCL12-CXCR4 axis on cancer stem cells (CSCs) in GBM. GBM is the most well-known and most harmful essential glial tumor in grown-ups, portrayed by a perpetually poor result and constrained helpful choices (Dolecek et al., 2012). Standard GBM the executives includes maximal careful resection, trailed by radiotherapy with attending and adjuvant chemotherapy with temozolomide, however by and large GBM quickly backslides. Accessible medicines at backslide are to a great extent ineffectual and middle by and large endurance of GBM patients is around 15 months. There is expanding proof that tumor improvement, development, repeat and protection from chemo-and radio-treatment is identified with the nearness of a cell subpopulation, named malignancy undifferentiated organisms (CSCs), these days distinguished in various human hemopoietic and strong diseases, including GBM. Proficient CSC destruction speaks to the ineludible objective to forestall tumor backslide and along these lines an objective for all new anticancer methodologies.