These results, while confirming the expected individual differences within GBM CSC cultures, which reflect the distinct biological behavior and molecular heterogeneity (mutations in EGFR, IDH1, IDH2, etc.)of the original tumor, highlight how some GBM CSCs can be dependent on chemokines for proliferation and migration, and that these could be supplied not only by autocrine mechanisms but also by cells within the tumor stroma (or the CSC niche), including MSCs. This evidence concerns the gene IDH1 and neoplasm.