In addition to being quiescent, CSCs maintain low reactive oxygen species (ROS) levels, further contributing to CSC survival and recurrence potential.108 Unlike non-CSCs, which accumulate toxic ROS and undergo apoptosis, CSCs activate antioxidant defense systems, including superoxide dismutase (SOD), glutathione peroxidase (GPX), glutathione (GSH), and catalase (CAT), to mitigate the oxidative stress induced by cytotoxic therapy.109 ROS regulation not only enhances CSC survival posttreatment but also preserves cancer stemness, facilitating tumor recurrence. This evidence concerns the gene SOD1 and neoplasm.