LYG1 (Lysozyme G-like 1) is a classical secretory protein with dual roles in immune regulation and tumor control. Functionally, LYG1 promotes CD4+ T cell activation, proliferation, and interferon-gamma (IFN-γ) production 1, driving antitumor immune responses. In tumor models, recombinant LYG1 protein suppressed B16 melanoma growth in wild-type mice through CD4+ T cell-dependent mechanisms, with effects abolished in immunodeficient mice or IFN-γ-knockout animals 1. LYG1 deficiency accelerated tumor growth and impaired T cell function, confirming its tumor-inhibitory role 1. Conversely, LYG1 drives pathogenic T cell responses in acute graft-versus-host disease (aGVHD). LYG1 deficiency in donor T cells attenuated aGVHD severity by reducing CD4+ T cell activation, suppressing IFN-γ production, promoting regulatory T cell (Treg) differentiation, and reducing chemokine-driven immune infiltration 2. Recombinant LYG1 administration exacerbated aGVHD through IFN-γ-dependent mechanisms 2. Clinically, LYG1 expression associates with thyroid tumor classification; LYG1 mRNA serves as a molecular marker in a four-gene panel (with OCLN, ZNF423, AQP5) for identifying non-invasive follicular thyroid neoplasms 3. Additionally, LYG1 expression declines with kidney aging and associates with age-related renal dysfunction, suggesting roles in organ homeostasis 4.