CXCR2 and glioblastoma: Thus, a completely different scenario can be drawn as far as UC-MSC modulation of GBM CSCs proliferation, according to the occurrence of a direct interaction between the different cell populations (mainly showing antiproliferative activity, independent from cyto/chemokine release and CXCR2 activation), or when the interaction is mediated by soluble factors, and CXCR2 ligands in particular, which determine an opposite response (CSC proliferation and activation of migration).