In autophagy, the unique double membrane-bound autophagosomes transiently emerge in the cytoplasm, sequester portion of the cytosol and organelles, and eventually fuse with lysosomes to degrade the contents.In addition to the basic role in nutrient supply under starvation conditions, the process unexpectedly functions in suppression of various diseases including tumorigenesis, neurodegeneration, type Ⅱ-diabetes, infectious diseases, inflammatory diseases, etc.My group has been working on unraveling the molecular machinery and pathophysiology of mammalian autophagy for 18 years.LC3, a first protein we identified, has been mostly used golden marker in autophagy studies.This single paper has been cited in over 3,000 papers.Recently, we have provided new insights into biogenesis of autophagosome,which have been topic of longstanding debate.We showed that autophagosome forms at the ER-mitochondria contact site.Previously, we found that autophagy selectively eliminates invading pathogenic bacteria, opening a new field on host-pathogen interaction.Then, we unraveled that autophagy recognizes damage of endosomal membrane including bacteria rather than bacteria itself.We also found a new role of autophagy;suppression of nephropathy through selective elimination of damaged lysosomes.