COPS2 (COP9 signalosome subunit 2) is a multifunctional protein that plays critical roles in cellular regulation and pathological processes. As a component of the COP9 signalosome complex, COPS2 regulates protein stability through deneddylation and ubiquitination pathways 1. In pluripotency maintenance, COPS2 stabilizes Nanog protein by preventing proteasomal degradation and functions as a transcriptional corepressor, being essential for embryonic stem cell maintenance and somatic cell reprogramming 2. COPS2 demonstrates unique autophagy-hijacking capabilities, coordinating both autophagosome entry and autolysosome exocytosis for viral propagation by regulating K11/K48-linked ubiquitination and SNAP29 O-GlcNAcylation 1. In cancer contexts, COPS2 shows complex roles: it serves as a prognostic biomarker in bladder cancer 3, is downregulated in cancer cachexia but normalized by exercise training 4, and functions as a suppressor of break-induced replication, with its knockdown increasing genome instability and mutagenic hotspots 5. Additionally, COPS2 upregulation promotes cell proliferation in response to avian influenza infection 6, highlighting its diverse regulatory functions across development, disease, and cellular stress responses.