ATG10 is an E2-like conjugating enzyme essential for autophagy initiation. It catalyzes the transfer of ATG12 to ATG5, a critical step required for autophagosome assembly and the autophagic cascade. ATG10 is upregulated in specific lung epithelial cell subsets, particularly club cells, and participates in cellular stress responses across multiple tissues 1. The gene also plays a role in adenovirus-mediated cell lysis. ATG10 variants associate with distinct disease phenotypes. In a Chinese Guangxi population, ATG10 polymorphisms (rs1864182 and rs1864183) correlated with clinical manifestations in antineutrophil cytoplasmic autoantibody-associated vasculitis, including hemoptysis, hematuria, and proteinuria, though not directly with AAV susceptibility 2. Similarly, the ATG10 rs4703863 variant increased susceptibility to Vogt-Koyanagi-Harada (VKH) syndrome in a Chinese Han population, while the A allele was protective 3. Recent evidence suggests ATG10 may have tumor-relevant functions. ATG10 is downregulated in kidney chr5 carcinoma (KICH) and regulated by m6A RNA methylation, with its downregulation correlating with patient survival and implicating cuproptosis pathways 4. In hepatocellular carcinoma, ATG10 was identified as a component of exhausted CD8+ T cell-related prognostic signatures, potentially influencing immunotherapy responsiveness 5. ATG10 upregulation also occurs in models of neurodegeneration when trehalose promotes autophagy, suggesting therapeutic potential in neurodegenerative diseases 6.