It meticulously analyzes the processes by which redox imbalance and the activation of essential signaling pathways, namely Nrf2/Keap1, AKT/c-Myc, and Wnt/β-catenin, facilitate the survival, plasticity, and significant treatment resistance of GSCs, as well as the capacity of these cancer stem-like cells to adapt to oxidative stress and modify their metabolism, hence facilitating tumor proliferation and resistance to therapy. The gene discussed is MYC; the disease is neoplasm.