Even though exposure of tumor cells to HAMLET results in cytochrome c-release from mitochondria and activation of caspases, inhibitors of these pathways do not prevent cell death and cell death is not regulated by Bcl-2 or p53 family proteins [23], [24], demonstrating that the effects of HAMLET on cell viability are independent of common apoptosis effector molecules. The gene discussed is TP53; the disease is neoplasm.