COPS7B is a subunit of the COP9 signalosome (CSN), a multi-protein complex with critical roles in cellular protein regulation and disease pathogenesis. As a component of CSN, COPS7B primarily functions in protein deneddylation of cullin-based E3 ubiquitin ligases, thereby reducing their conjugation activity 1. The CSN complex also participates in phosphorylation of key regulatory proteins including p53 and JUN, modulating their degradation through the ubiquitin system. COPS7B exhibits a notable role in ribosome biogenesis and mRNA translation initiation, where it interacts with ribosomes to regulate protein synthesis rates 2. Additionally, COPS7B participates in global genome nucleotide excision repair (GG-NER) through BAP1-mediated deubiquitination, contributing to DNA damage recognition 3. Circadian clock function also depends partly on COPS7B-regulated protein stabilization, particularly of the circadian protein BMAL1 4. Clinically, elevated COPS7B expression serves as an independent prognostic biomarker in hepatocellular carcinoma and colorectal cancer, correlating with poor outcomes and immune infiltration 12. COPS7B has also been identified as a causally associated plasma protein affecting vascular dementia and HCC risk in genetic studies 56. These findings establish COPS7B as a multi-functional regulator with significant therapeutic potential across multiple cancer types and neurodegenerative diseases.