DEK is a chr6-remodeling oncoprotein with multifaceted roles in cellular regulation and disease. In cancer biology, DEK functions as an oncogene that is overexpressed in numerous malignancies and contributes to cellular transformation by affecting proliferation, differentiation, senescence, and apoptosis 1. DEK regulates B-cell proliferative capacity, with high expression correlating with increased tumor proliferation and inferior survival in low-grade B-cell lymphomas 2. The protein forms pathogenic fusion proteins, including DEK-AFF2 in aggressive sinonasal carcinomas that display distinctive histologic features despite bland morphology 3. Beyond oncology, DEK plays critical roles in chr6 organization and transcriptional regulation through epigenetic mechanisms 1. In the central nervous system, DEK expression is highest during fetal development and associated with pathways involved in DNA repair, cellular proliferation, synaptic transmission, and neurite outgrowth 4. DEK also contributes to immune regulation, as it can be targeted to reduce neutrophil extracellular trap formation (NETosis) in wound healing applications 5. The protein's involvement in DNA damage response and its age-related expression patterns suggest potential roles in neurodegeneration and brain aging 4.