Targeting MYC and mTOR signaling in medulloblastoma presents a promising approach to overcoming chemoradiation resistance, but several mechanisms of resistance could emerge in response to these treatments [129, 132] These mechanisms could either diminish the therapeutic effects of inhibitors targeting MYC and mTOR, or enable tumor cells to bypass the targeted pathways, thereby contributing to tumor persistence and recurrence [133]. This evidence concerns the gene MYC and neoplasm.