LAP3 is a cytosolic metallopeptidase that catalyzes removal of N-terminal hydrophobic amino acids from peptides, with zinc ions essential for its catalytic activity 1. The enzyme is involved in glutathione metabolism and redox homeostasis through glutathione S-conjugate degradation. LAP3 demonstrates significant pathological relevance across multiple disease contexts. In hepatocellular carcinoma, LAP3 is upregulated and correlates with poor prognosis, promoting cell proliferation through G1/S checkpoint regulation and enhancing cell migration and invasion 1. In non-alcoholic fatty liver disease (NAFLD), cholesterol-dependent LAP3 upregulation inhibits hepatocyte autophagy, with serum LAP3 levels correlating positively with triglycerides and gamma-glutamyltransferase while negatively correlating with HDL levels 2. LAP3 also promotes glioma progression by enhancing cell viability, proliferation, migration, and invasion 3. In breast cancer pathogenesis, LAP3 mediates IFN-γ-induced arginine depletion through interference with argininosuccinate synthetase (ASS1), driving malignant transformation via HDAC2 upregulation and cell cycle protein expression 4. Additionally, LAP3 has been identified as a potential druggable inflammatory target in COVID-19 hyperinflammation 5 and is associated with viral immunosuppression in rhinovirus-induced asthma 6. Clinically, LAP3 represents a promising biomarker and therapeutic target for liver disease, hepatocellular carcinoma, glioma, and breast cancer.