In addition, increased mitochondrial ROS levels drive “mitohormesis”, a condition of mild mitochondrial stress that favours pro-survival pathways through the activation of mammalian target of rapamycin (mTOR) complex 1 (mTORC1) signalling, an alteration that is frequently associated with poor clinical outcome of cancer patients.22 Notably, the mitochondria-targeted O2•– scavenger mitoTEMPO inhibits tumour cell migration and metastasis in mice,23 corroborating a crucial role for ETC-derived O2•– in tumorigenesis. This evidence concerns the gene MTOR and neoplasm.