Inhibition of SMO represents a promising strategy to overcome therapy resistance in HGG; the Smoothened inhibitor cyclopamine has been shown to induce radiosensitization in glioblastoma cells and Erismodegib, another SMO inhibitor, was capable of inhibiting self-renewal and EMT in glioblastoma initiating cells [211, 212]. This evidence concerns the gene SMO and glioblastoma.