From the mechanistic viewpoint, preferential sensitivity of GSC-driven tumors with mutated TP53 is consistent with the concept of synthetic lethality [84], whereby the combination of two inactivating events (p53 mutation and AKT inhibition, in the context of our study) is a prerequisite of effective outcome (ClQ-mediated tumor radiosensitization). This evidence concerns the gene AKT1 and neoplasm.