Cancer cells with increased oxidative stress are more vulnerable to damage by further ROS elevation induced by exogenous agents, which can induce apoptosis and cell cycle arrest in cancer cells partly mediated by the p53 signaling pathway.14,16 Then, it is feasible to selectively kill cancer cells via ROS manipulating, without causing significant toxicity to normal cells.14 The underlying target protein of Celastrol, which is able to manipulate the redox homeostasis in various cancer cells, is promising for the anti-tumor drug discovery and development. This evidence concerns the gene TP53 and cancer.