The pro-apoptotic protein Apaf1 (apoptotic protease activating factor 1) forms the core of the apoptosome and is a crucial component of the mitochondria-dependent death pathway. Paradoxically, Francesco Cecconi and colleagues (p. 3450) now report that, by regulating centrosome morphology and function, Apaf1 also has a pro-survival role. By analysing Apaf1-depleted cells, the authors show that Apaf1 loss induces defects in the centrosome, the major microtubule organizing centre in animal cells. These defects impair centrosomal microtubule nucleation and cytoskeleton organization, thereby affecting mitotic spindle formation, cell migration and mitochondrial network organization. As a result, Apaf1-depleted cells are more fragile and have a lower stress response threshold than wild-type cells. Apaf1 regulates centrosome maturation, the authors report, by controlling the recruitment of HCA66 (hepatocellular carcinoma antigen 66) to the centrosome; HCA66, a positive regulator of Apaf1-dependent apoptosis, is also required for the stability of the γ-tubulin small complex that helps to form the pericentriolar material in the centrosome. Together, these results suggest that Apaf1 is a pro-survival protein, as well as a pro-apoptotic protein. Thus, Apaf1 could help to regulate the equilibrium between cell death and survival.