LGALS7 (galectin-7) is a β-galactoside-binding protein preferentially expressed in skin tissue that functions as a multivalent regulator of epithelial biology and immune homeostasis 1. Intracellularly, LGALS7 acts as a pro-apoptotic protein that activates JNK signaling and triggers mitochondrial cytochrome c release 1. The protein also contributes to epithelial cell differentiation, migration, and wound re-epithelialization 1. In cancer, LGALS7 demonstrates context-dependent roles: it promotes non-melanoma skin cancer development by binding CD11b+ myeloid cells and enhancing their immunosuppressive function through increased IL-10 and TGF-β1 secretion 2, while serving as an immune evasion marker downregulated by tumor-suppressing ncRNAs in colorectal cancer 3. In Stevens-Johnson syndrome/toxic epidermal necrolysis pathogenesis, LGALS7 interacts with TRPM2 to trigger mitochondrial dysfunction and keratinocyte apoptosis via DRP-1-dependent fission 4. Genetically, LGALS7 promoter polymorphisms (rs567785577, rs138945880) associate with intracerebral hemorrhage stroke risk 5, and circulating LGALS7 levels causally impact estimated glomerular filtration rate 6. Galectin-7-specific nanobodies show promise for cancer immunotherapy by blocking T-cell apoptosis 7.