ROS exert dual roles depending on their concentration: at moderate levels, they act as signaling molecules, activating survival and proliferative pathways such as PI3K/AKT/mTOR and MAPK (mitogen-activated protein kinase) cascades; at high levels, they cause DNA damage, genomic instability, and oxidative modification of cellular macromolecules, thereby fostering tumor heterogeneity and therapeutic resistance [37,38]. This evidence concerns the gene AKT1 and neoplasm.