Cell autophagy is an important physiological phenomenon in biology. The so-called autophagy refers to the process in which cells form a double-layer membrane sac structure called autophage, wrap a part of cytoplasm, and transport it to lysosome for degradation and recycling. There are two main functions of autophagy: one is that under stress, autophagy can degrade some cytoplasm into amino acids, providing energy and materials for cell survival, which is a self survival mechanism of cells; The second is to remove the "garbage" such as misfolded proteins, aging or damaged organelles to maintain the normal functions of cells and the body. Therefore, autophages are also called "cell scavengers". If autophagy is abnormal, it will lead to the accumulation of "garbage" in cells, leading to a variety of diseases, such as Alzheimer's disease, Parkinson's disease, amyotrophic lateral sclerosis (commonly known as involution) and other neurodegenerative diseases. Therefore, the in-depth study of autophagy is helpful to reveal the pathogenesis of related diseases and develop new diagnostic and therapeutic methods. So, how did autophage, the "cell scavenger" in multicellular organisms come into being? Zhang Hong's research group of Institute of Biophysics, Chinese Academy of Sciences recently published their latest research results in the journal Cell, which attracted attention from international peers. This study shows that the calcium transient on the surface of the endoplasmic reticulum is the starting signal of autophagy, which opens a new direction in the study of autophagy initiation. Zhang Hong introduced that autophagy is highly conservative in multicellular organisms. Moreover, multicellular autophagy is far more complex than that of unicellular yeast autophagy, including many unique steps. For example, in multicellular organisms, autophages are formed on the endoplasmic reticulum rather than lysosomes. It can be inferred that there are unknown important genes involved in the formation of multicellular autophage. Finding a multicellular biological model suitable for genetic screening to screen new autophagic genes is of great significance for further exploring the molecular mechanisms of these processes. Zhang Hong's research team found that P granule protein from oocytes can be removed by autophagy during embryonic development. This discovery established the first multicellular autophagy research system suitable for genetic screening. Using this model, the research team identified a number of new autophagic genes unique to multicellular organisms - EPG genes through genetic screening. Further studies have found that these new genes play a role in the specific steps of autophagy in multicellular organisms, greatly enriching people's understanding of autophagy in multicellular organisms. Zhang Hong's research team found that in multicellular organisms, under autophagy induction conditions, FIP200/ATG13/ULK1 complex (corresponding to the ATG1 complex of yeast) forms aggregates on the endoplasmic reticulum, and then recruits downstream autophagic proteins to start the formation of autophages. So, what signals does the endoplasmic reticulum release to cause FIP200 complex to form aggregates? This is a long pending scientific problem in the field of autophagy. "After years of research, we found the answer to this question." According to Zhang Hong, their research found that autophagy induced calcium transient/calcium oscillation on the surface of endoplasmic reticulum, which caused FIP200 complex to form condensation through liquid-liquid phase separation