Programmed cell death (PCD) is usually thought to occur by one of two mechanisms. Type I PCD (apoptosis) involves the enzymes caspases and is characterized by chromatin condensation and nuclear fragmentation. Type II is instead characterized by accumulation of autophagic vacuoles, which sequester cytosol and organelles during autophagy (a survival response used to combat nutrient deprivation). But how distinct are type I and type II PCD and what is the real relationship between type II PCD and autophagy? Guido Kroemer and co-workers have examined PCD in nutrient-deprived cells lacking the lysosomal protein LAMP2. These have increased numbers of autophagic vacuoles, because fusion of these vacuoles with lysosomes is inhibited (see p. 3091). The authors find that, despite accumulation of autophagic vacuoles, the PCD that occurs displays numerous hallmarks of apoptosis, such as loss of mitochondrial potential, caspase activation and chromatin condensation. Moreover, they can block it with caspase inhibitors and agents that stabilize mitochondria. The authors conclude that cells that accumulate autophagic vacuoles can progress to apoptosis. They therefore argue that the two types of PCD are not as distinct as many thought.