Ebf1, also known as early B cell factor 1, is a crucial transcription factor. It plays a vital role in early B cell lymphopoiesis, acting as a key regulator of B cell specification [1,2,4,5]. Ebf1 is involved in processes like establishing and stabilizing chromatin accessibility in lymphoid progenitors and pro-B cells, which is essential for lineage-specific gene expression changes during B cell differentiation [3,5]. It also participates in the regulation of genes related to V(D)J recombination, a process fundamental to the development of a diverse lymphocyte antigen receptor repertoire in adaptive immunity [1,2].

In gene knockout (KO) mouse models, Ebf1 deficiency leads to significant impacts on B cell development. Acute protein degradation in mice revealed that Ebf1, along with other transcription factors, controls early B cell lymphopoiesis. Ebf1 predominantly functions as a transcriptional activator, inducing open chromatin at its target genes such as Igll1 and Vpreb1 in pro-B cells [1]. In pro-B cells, replacing Ebf1 with a degradable form showed that continuous Ebf1 activity is required for maintaining the transcriptional and epigenetic state of these cells [3]. Additionally, in hematopoietic cells, Ebf1 deletion enhanced myelopoiesis and reduced HSC repopulation capacity, suggesting its role in regulating myeloid/lymphoid fate bias in multipotent progenitors [6].

In conclusion, Ebf1 is essential for early B cell development, influencing chromatin accessibility, gene expression, and the balance between myeloid and lymphoid lineages. The use of KO mouse models has been instrumental in uncovering these functions, providing insights into the pathogenesis of B-cell-related hematologic neoplasms and potentially other diseases associated with abnormal B cell development [1,2,6].