ZNF592 is a zinc finger transcription factor involved in multiple biological pathways. It functions as a DNA-binding protein with transcriptional regulatory capacity 1. ZNF592 is a component of the Z4 protein complex that associates with BRD4-NUT oncogenic fusions, and evidence suggests it participates in protein-protein interactions within nuclear foci 2. The protein can be targeted for degradation through ubiquitin-proteasome pathways in response to specific regulatory signals 3. Disease relevance spans multiple conditions. ZNF592 mutations cause CAMOS (Cerebellar Ataxia with Mental retardation, Optic atrophy and Skin abnormalities), a rare autosomal recessive syndrome; a p.Gly1046Arg missense mutation in the eleventh zinc finger domain disrupts DNA-binding properties and impairs cerebellar development 1. Rare variants in ZNF592 are significantly associated with progressive supranuclear palsy (PSP), a neurodegenerative tauopathy 45. ZNF592 also functions as a fusion partner in NUT carcinoma, where ZNF592-NUTM1 fusions drive aggressive malignancy, indicating oncogenic potential when translocated 26. Additionally, novel gene fusions involving ZNF592 have been identified in myelodysplastic neoplasia 7. Clinically, ZNF592 represents a potential therapeutic target in NUT carcinoma and may inform understanding of neurodegenerative disease mechanisms.