Notably, a large accumulation of ROS represses tumor growth through two mechanisms: (1) by blocking the signaling pathway responsible for cancer cell proliferation, as well as the cell cycle and the biosynthesis of ATP and nucleotides; and (2) by promoting tumor cell death via activating the p53-independent, mitochondrial, and endoplasmic reticulum stress–apoptotic pathways and the ferroptosis pathway [46]. This evidence concerns the gene TP53 and neoplasm.