IFI6 and cancer: A burst of mtROS was implicated in opening of mitochondrial permeability transition pore (MPTP) to induce apoptosis and low-to-moderate mtROS levels were suggested to foster cancer progression.14, 15 Despite increased mtROS, mitochondria of G1P3-overexpressing cells were intact (Fig. 2c), slightly hyperpolarised and maintained the mtΔΨ under apoptotic stress.2, 3 These results suggested that in MCF-7G1P3 cells, mtROS levels were not high enough to open MPTP or mtROS-mediated apoptosis was neutralised.