Mitochondria are not only the powerhouse of the cell, but are also involved in cellular suicide via apoptosis (programmed cell death). This pathway is a major regulator in cell death where pro- and anti-survival Bcl-2 proteins meet at the mitochondrial outer membrane and decide the fate of a cell. Treatment-resistant tumour cells often possess mitochondria which are enriched in the pro-survival Bcl-2 membrane protein which blocks any killing (anti-survival) protein like BAX. Based on recent NR studies we will now investigate how the killer Bax protein interacts with mitochondrial-like membranes upon oxidative stress and how it will be inhibited in the presence of pro-survival Bcl-2 protein there. Information about this key protein complex is essential to understand the regulation of the cell's fate: why do healthy cells survive, damaged cells get removed and cancer cells escape.