DEK, a highly conserved nuclear factor, is an oncogene that has been found fused with genes like NUP214 in acute myeloid leukemia, and is overexpressed in many cancers [1,2,4]. It plays crucial roles in multiple cellular processes such as self-renewal, proliferation, differentiation, senescence, and apoptosis [4]. DEK also seems to be involved in epigenetic and transcriptional regulation, although the exact mechanisms are complex and not fully understood [4].

In hematopoietic stem cells (HSCs), nuclear DEK is essential. HSCs lacking DEK show defects in long-term self-renewal capacity, reduced quiescence, and accelerated mitochondrial metabolism, which is in part due to activating mTOR signaling [1]. DEK deficiency leads to reduced chromatin accessibility in HSCs, affecting the expression of quiescence-associated genes [1].

In asthma, DEK deficiency alleviates airway inflammation by down-regulating PINK1-Parkin mitophagy, NLRP3 inflammasome activation, and apoptosis, potentially through the DEK/ATAD3A/DRP1 signaling axis [3].

In summary, DEK is vital for normal cellular functions, especially in maintaining the potential of HSCs. Its dysregulation is associated with various diseases including leukemia, squamous cell carcinoma, breast cancer, and asthma. The study of DEK knockout models has provided insights into its role in these disease conditions, helping to understand disease mechanisms and potentially identify new therapeutic targets.