The article provides a historical overview of autophagy research, highlighting key milestones and contributions. The term "autophagy" was coined by C. de Duve in 1963 to describe the degradation process of cytoplasmic constituents in lysosomes/vacuoles. Early studies using electron microscopy revealed autophagy as a means of delivering intracellular components to lysosomes. However, significant molecular advances in understanding autophagy did not occur until the early 1990s when autophagy was discovered in yeast under starvation conditions. Genetic screens identified many autophagy-defective mutants, leading to the identification of autophagy-related genes (ATGs) in yeast. These genes revealed unique sets of molecules involved in membrane dynamics during autophagy, and their conservation across various organisms indicated that autophagy is a well-conserved mechanism among eukaryotes. The discovery of ATGs and their functional units, such as the Atg12 conjugation system, the Atg8 lipidation system, and the PI-3K complex, provided a molecular framework for understanding autophagosome formation. The identification of homologs of ATGs in mammals and other organisms further facilitated research. Genetic manipulation in mice, such as the generation of GFP-LC3 transgenic mice and Atg5 knockout mice, has been crucial for studying autophagy in higher eukaryotes. Autophagy plays a crucial role in protein turnover, nutrient recycling, and cellular homeostasis. It is essential for survival during fasting and nutrient deprivation. The involvement of autophagy in various physiological processes and diseases has also been extensively studied, leading to a deeper understanding of its broader roles in health and disease. The article emphasizes the importance of yeast as a model organism in advancing the field of autophagy research.The article provides a historical overview of autophagy research, highlighting key milestones and contributions. The term "autophagy" was coined by C. de Duve in 1963 to describe the degradation process of cytoplasmic constituents in lysosomes/vacuoles. Early studies using electron microscopy revealed autophagy as a means of delivering intracellular components to lysosomes. However, significant molecular advances in understanding autophagy did not occur until the early 1990s when autophagy was discovered in yeast under starvation conditions. Genetic screens identified many autophagy-defective mutants, leading to the identification of autophagy-related genes (ATGs) in yeast. These genes revealed unique sets of molecules involved in membrane dynamics during autophagy, and their conservation across various organisms indicated that autophagy is a well-conserved mechanism among eukaryotes. The discovery of ATGs and their functional units, such as the Atg12 conjugation system, the Atg8 lipidation system, and the PI-3K complex, provided a molecular framework for understanding autophagosome formation. The identification of homologs of ATGs in mammals and other organisms further facilitated research. Genetic manipulation in mice, such as the generation of GFP-LC3 transgenic mice and Atg5 knockout mice, has been crucial for studying autophagy in higher eukaryotes. Autophagy plays a crucial role in protein turnover, nutrient recycling, and cellular homeostasis. It is essential for survival during fasting and nutrient deprivation. The involvement of autophagy in various physiological processes and diseases has also been extensively studied, leading to a deeper understanding of its broader roles in health and disease. The article emphasizes the importance of yeast as a model organism in advancing the field of autophagy research.