CSPG4 and glioma: We further analyzed CSPG4 function in relation to integrin signaling in the GIC differentiation and tried to demonstrate the possibility that CS-modified CSPG4 maintains GIC stemness by forming a specific microenvironment for GICs, the so-called “glyco-niche,” which inhibits the switching on the integrin-related differentiation/stimulation to the glioma development, and thus, CS, CSPG4, and the associating integrin signaling could be promising GIC therapy targets.