This review discusses the autophagy pathway, a cellular process that allows cells to degrade intracellular components. The process involves the formation of a double-membrane structure called the autophagosome, which then fuses with lysosomes for degradation. The review outlines the molecular mechanisms involved in autophagosome formation, including the role of ATG proteins, the ER, Golgi complex, and endosomes. It also covers the role of membrane contacts, lipid droplets, and the ER-Golgi intermediate compartment in autophagosome formation. The review highlights the importance of SNARE proteins, tethering factors, and the autophagic lysosome reformation process in autophagosome-lysosome fusion. The review also discusses the role of various proteins and lipids in this process, as well as the regulation of autophagy by signaling pathways such as mTOR. The review concludes by emphasizing the importance of understanding the molecular details of autophagy for the development of therapeutics targeting autophagy in human diseases.This review discusses the autophagy pathway, a cellular process that allows cells to degrade intracellular components. The process involves the formation of a double-membrane structure called the autophagosome, which then fuses with lysosomes for degradation. The review outlines the molecular mechanisms involved in autophagosome formation, including the role of ATG proteins, the ER, Golgi complex, and endosomes. It also covers the role of membrane contacts, lipid droplets, and the ER-Golgi intermediate compartment in autophagosome formation. The review highlights the importance of SNARE proteins, tethering factors, and the autophagic lysosome reformation process in autophagosome-lysosome fusion. The review also discusses the role of various proteins and lipids in this process, as well as the regulation of autophagy by signaling pathways such as mTOR. The review concludes by emphasizing the importance of understanding the molecular details of autophagy for the development of therapeutics targeting autophagy in human diseases.