Autophagy is a primordial and highly conserved intracellular process that occurs in most eukaryotic cells and participates in stress management. This pathway involves the de novo formation of vesicles called autophagosomes, which can engulf entire regions of the cytoplasm, individual organelles, protein aggregates, and invading pathogens ( Figure 1 ). The autophagosomes fuse with endosomal compartments to form amphisomes prior to fusion with the lysosome, where their contents are degraded and the resulting metabolites are recycled back to the cytoplasm (Figure 1 ). Unique features of the pathway include the double-membrane structure of the autophagosomes, which were originally characterized over 50 years ago from detailed electron microscopy studies [5] . Starting in the 1990s yeast mutational studies began the genetic and molecular characterization of the key components required to initiate and build an autophagosome In response to inactivation of mTORC1 (but also other cellular and environmental cues), the ULK1 complex is activated and translocates in proximity of the endoplasmic reticulum (ER). Thereafter, the ULK1 complex regulates the class III PI3K complex. Atg9L, a multimembrane spanning protein, is also involved in an early stage of autophagosome formation by probably supplying part of the membranes necessary for the formation and/or expansion. Local formation of PI3P at sites called omegasomes promotes the formation of the phagophore, from which autophagosomes appear to be generated. The PI3P-binding WIPI proteins (yeast Atg18 homolog), as well as the Atg12-Atg5-Atg16L1 complex and the LC3-phosphatidylethanolamine (PE) conjugate play important roles in the elongation and closure of the isolation membrane. Finally, the complete autophagosome fuses with endosomes or endosome-derived vesicles forming the amphisome, which subsequently fuses with lysosomes to form autolysosomes. In the lysosomes, the cytoplasmic materials engulfed by the autophagosomes are degraded by resident hydrolases. The resulting amino acids and other basic cellular constituents are reused by the cell; when in high levels they also reactivate mTORC1 and then suppress autophagy. [6] . Subsequently, genetic and transgenic studies in plants, worms, fruit flies, mice, and humans have underscored the pathway's conservation and have begun to unveil the intricate vital role that autophagy plays in the physiology of cells and multicellular organisms.