LGALS8 (galectin-8) is a beta-galactoside-binding lectin functioning as a critical sensor of membrane damage during pathogenic infection 1. Upon bacterial or viral infection, LGALS8 detects endosomal membrane rupture by recognizing beta-galactoside ligands exposed to the cytoplasm and initiates xenophagy through interaction with CALCOCO2/NDP52, restricting Salmonella typhimurium and Picornaviridae replication 12. Beyond canonical autophagy, LGALS8 contributes to cellular stress responses by recruiting to damaged lysosomes where it cooperates with NUFIP2 to inactivate mTORC1 via the Ragulator-RRAGA-RRAGB complex, promoting autophagy reinforcement 34. In glioblastoma, hypoxia-induced LGALS8 maintains cancer stem cell stemness through mTOR inactivation and TFEB-mediated autophagic lysosomal biogenesis, correlating with poor prognosis 4. Conversely, LGALS8 exhibits pro-tumorigenic functions in multiple contexts: it inhibits FGFR1 endocytosis, stabilizing receptor signaling 5, and induces immunosuppressive cytokine secretion (IL-6, IL-1β, RANKL, MCP-1) through MRC2/uPAR/LRP1 and integrin ligation, promoting the cytokine storm phenotype 6. LGALS8 dysregulation is associated with metastatic progression in non-small cell lung cancer and gastric cancer, implicating it as both a pathogen defense mechanism and a cancer-promoting factor depending on cellular context.