Bcl6b, also known as BAZF, ZBTB28, and ZNF62, operates as a sequence-specific transcriptional repressor in the nucleus. It plays crucial roles in multiple biological functions such as tumor suppression, immune response, stem cell self-renewal, and vascular angiogenesis [2]. It is also involved in pathways like VEGF and Notch signaling, which are important for processes like angiogenesis and endothelial cell function [1].

In ocular vascular diseases, Bcl6b-deficient endothelial cells showed Notch signal activation and attenuated cord formation via blocking the VEGF-VEGFR2 signaling pathway. Bcl6b-targeting small-interfering ribonucleic acid decreased choroidal neovascularization lesions and suppressed ocular edema in the neuroretina, suggesting it may be a therapeutic target for such diseases [1]. In endothelial cell differentiation, overexpression of Bcl6b suppressed while knockdown improved the differentiation from human induced pluripotent stem cells (hiPSCs), and it inhibited the process by repressing the transcriptional activity of ETV2 [2]. In gastric cancer, knockout of Bcl6b in mice worsened the disease severity and aggravated the inflammatory response, while re-activation of Bcl6b impeded inflammatory amplification and tumor development [3].

In conclusion, Bcl6b has diverse biological functions including its role in ocular vascular diseases, endothelial cell differentiation, and gastric cancer development. Gene knockout models in mice have been instrumental in revealing its functions in these specific disease areas, highlighting its potential as a therapeutic target for certain diseases.