In conclusion, SM acted as a pro-oxidant to suppress tumor-like symptom induced by over-activated ras. It regulated CypD of PTP on mitochondrial membrane to induce the generation superoxide anion, and increase the accumulation of ROS, finally cause severe oxidative stress to suppress the over-activated Ras/MAPK pathway, and p53, JNK, and p38/MAPK were all involved in the action of SM. The gene discussed is TP53; the disease is neoplasm.