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. This evidence concerns the gene CSPG4 and central nervous system cancer.