AGBL4 is a metallocarboxypeptidase that catalyzes protein deglutamylation, primarily removing polyglutamate side chains from tubulin and non-tubulin proteins 1. The enzyme specifically cleaves tubulin long-side-chains while preserving the branching point glutamate, and also deglutamylates non-tubulin substrates including MYLK and KLF4 1. AGBL4-mediated KLF4 deglutamylation promotes proteasome-mediated degradation, negatively regulating cell pluripotency and embryogenesis 1. Beyond tubulin modification, AGBL4 plays roles in neuronal differentiation 2 and immune responses. In disease contexts, AGBL4 upregulation promotes glioblastoma malignant progression through modulation of MMP-1 and inflammatory pathways; AGBL4 knockdown inhibits GBM cell proliferation, migration, and invasion 3. AGBL4 expression differences distinguish non-progressive from progressive sarcoidosis in bronchoalveolar lavage cells, suggesting involvement in disease progression mechanisms 4. Additionally, AGBL4 genetic variants associate with cardiometabolic risk, including lipid metabolism alterations in population-specific haplotypes 5. AGBL4 polymorphisms correlate with susceptibility to antituberculosis drug-induced hepatotoxicity, with population-specific genotype frequencies affecting DILI risk in Peruvian subpopulations 67. Clinically, AGBL4 represents both a potential biomarker and therapeutic target for managing cancer progression, inflammatory diseases, and adverse drug reactions.