Bcl6, also known as B-cell lymphoma 6, is a transcriptional repressor that plays a crucial role in the development and maintenance of germinal centers (GCs), which are essential for an effective humoral immune response [2]. It is also involved in many other biological processes such as cell proliferation, survival, differentiation, migration, and invasion [1]. Genomic aberrations of Bcl6 can lead to the development of GC-derived lymphomas and it is considered a key oncogene in various cancers [2,5].

In mouse models, deletion of Bcl6 in lymphoid tissue inducer-like ILC3s resulted in dysregulation of the transcriptional program and enhanced expression of interleukin-17A (IL-17A) and IL-17F, associated with worsened inflammation in a colitis model, indicating its role in ILC3 subset biology [4]. In gastrointestinal stromal tumor (GIST) cells, induction of Bcl6 by imatinib mesylate (IM) treatment led to suppression of apoptosis and IM resistance. Targeting Bcl6 with an inhibitor, BI-3802, restored IM sensitivity and showed synergy with IM in vitro and in vivo, suggesting Bcl6's role in IM resistance [3].

In conclusion, Bcl6 is a critical regulator in immunity and tumorigenesis. Its functions in immune cell development, especially in GCs, are well-established. In disease areas such as lymphoma, GIST, and pre-eclampsia, studies using gene knockout or conditional knockout mouse models have revealed its roles in promoting tumor progression, drug resistance, and placental/endometrial pathophysiology, providing potential therapeutic targets for these diseases [1,2,3].