CHMP4B (charged multivesicular body protein 4B) is an ESCRT-III complex component essential for membrane fission and cellular homeostasis. Functionally, CHMP4B mediates intraluminal vesicle formation in endosomes and facilitates autophagosome-lysosome fusion through interaction with ALIX and other ESCRT machinery 1. CHMP4B regulates cytokinesis control and participates in exosome biogenesis, particularly tetraspanin sorting 1. Mechanistically, CHMP4B functions in lysosomal quality control and autophagy regulation. It interacts with IST1 to promote ESCRT-III assembly and autophagosome-lysosome fusion 2, and is controlled by HSP90β-mediated regulation 3. During pathological stress, CHMP4B activation initiates cell repair machinery in response to pyroptosis and oxidative damage 4. PRP4K regulates CHMP4B expression through splicing, controlling autophagosome-lysosome fusion in an evolutionarily conserved manner 5. Clinically, CHMP4B dysfunction associates with cataract formation; HSP90β downregulation causes CHMP4B upregulation, leading to excessive lens epithelial cell division and p53-mediated apoptosis 3. CHMP4B dysregulation also contributes to intervertebral disc degeneration through autophagy impairment 6 and kidney stone formation via insufficient cell repair 4. CHMP4B overexpression protects against these pathologies, highlighting its therapeutic potential. Additionally, CHMP4B is exploited by viruses (CSFV, HIV) for membrane remodeling and viral release 78.