Their molecular chemopreventive action, according to the available literature, occurs in multiple ways, i.e., through oxidative control of the cell (maintenance of oxidative–antioxidant homeostasis), suppression of neoangiogenesis and proliferation, as well as through cell cycle arrest, increased expression of the p53 protein (the most crucial suppressor of tumor transformation), and the subsequent induction of autophagy in cancer-altered cells [6,7]. The gene discussed is TP53; the disease is neoplasm.