Studies indicated that CRC cells with MT P53 were more chemo-resistant than those with WT p53 due to their poor ability to activate apoptosis and initiation of apoptosis is the most important functions of P53.34, 35 Thus, we hypothesized that oridonin preferentially induced cell death through apoptosis in WT P53 cancer cells, whereas in those MT P53 cancer cells oridonin triggered another mechanism (e.g., autophagy) to compensate for the low apoptotic activity. The gene discussed is TP53; the disease is cancer.