By preventing the massive death caused by ROS-dependent opening of the mitochondrial PTP, TRAP1 might favor the primary accretion of the tumor, and indeed we observe that mitochondrial superoxide levels increase during the focus forming assay in cells with low TRAP1 levels, and that ROS scavengers rescue the in vitro tumorigenicity of shTRAP1 cells. The gene discussed is TRAP1; the disease is neoplasm.