Autophagy is a highly conserved catabolic process that serves as a quality control mechanism in cells by selectively removing damaged and superfluous organelles or other harmful cytosolic material, such as aggregated proteins or invaded bacteria. Under stress or energy restriction autophagy provides recycled building blocks for the synthesis of new cellular components. Three different types of autophagy can be distinguished: macroautophagy, microautophagy and chaperone-mediated autophagy. This SFB focuses on macroautophagy (hereafter referred to as autophagy), a multi-step cellular process by which cytosolic material is engulfed by a double-membrane, termed autophagosome after closure, which eventually fuses with a lysosome in order to eliminate its content. Autophagy plays a vital role in protecting against disease, but in recent years it became clear that the effect of autophagy is highly contextual. While it acts for instance as an anti-tumorigenic mechanism in healthy cells, cancer cells exploit the cytoprotective effect of autophagy to overcome stress conditions and nutrient limitation caused by rapid tumor growth. SFB 1177 aims at gaining a more detailed insight into the mechanistic details of autophagic pathways to better understand its role in disease development and eventually exploit this knowledge therapeutically.