In the last decade a progress has been achieved in understanding the mechanisms which control the cell death. Accumulating evidence suggest that apoptosis is not the only one type of pro- grammed cell death (PCD). Cells use different pathways to active self-destruction process. There are three types of programmed cell death (PCD): condensation prominent, type I or apoptosis, dependent on the activity of caspases, type II – autophagy prominent and type III occurring through disintegration of cells into fragments without condensation and involvement of lysosomal system. Autophagy is a philo-genetically very old process, usually considered as a route of cellular proteins degradation and organelle turnover, comprising macroautophagy, microautophagy and chaperone-mediated autophagy. APG and AUT genes regulate this process in mammalian cells. Beclin 1, a homolog of the yeast autophagy protein Atg6 is required for vacuolar transport and can induce autophagy in human cells. Another one homolog of yeast Atg8 gene codes the microtubule-associated protein I (MAP I) light chain 3 (LC3) which exists on the autophagosomes and is currently the only reliable biochemical marker of autophagosomes. Autopha- gy is beneficial for the maintenance of the balance between the biosynthesis and catabolism of macromo- lecules and cell survival. On the other hand, autophagy is also involved in elimination of cancer cells by triggering a non-apoptotic cell death program (PCD II), indicating its inhibitory role in tumor develop- ment. This article reviews current knowledge on the role of autophagy in cancer cells and its dual function as a tool of cell protecting or killing. Authors emphasized molecular links between apoptosis and autopha- gy in tumor cells and possibility of their control for progression in anticancer therapy.