Zbtb33, also known as Kaiso, is a multi-functional transcriptional regulator. It belongs to the BTB/POZ family and has been implicated in various biological processes. It may be involved in pathways such as DNA methylation, RNA splicing, cell cycle regulation, and is important for proper development of animal embryos [2,3,5].

Zbtb33-edited mouse hematopoietic stem and progenitor cells showed a competitive advantage in vivo and increased genome-wide intron retention, suggesting its role in clonal hematopoiesis and myelodysplastic syndromes [1]. Zbtb33 gene knockout in mice led to increased locomotion, exploration, and pre-pulse inhibition, along with changes in the volumes of lateral ventricles and norepinephrine concentration in specific brain regions, indicating its involvement in the regulation of behavior and the central nervous system [4]. In the developing mouse brain, Zbtb33 gene knockout affected the transcription of genes related to the Wnt/β-catenin signaling pathway, such as Fgf9, Fgfr3, c-Myc, and FoxG1 [3].

In conclusion, Zbtb33 is crucial for multiple biological processes. Studies using Zbtb33 gene knockout mouse models have revealed its significance in clonal hematopoiesis, myelodysplastic syndromes, behavior, and central nervous system development, providing valuable insights into these complex biological systems and related disease areas.