BCL6 is a transcriptional repressor essential for germinal center (GC) formation and antibody affinity maturation 12. As the lineage-defining transcription factor for T follicular helper (Tfh) cells, BCL6 promotes Tfh differentiation while inhibiting Th1, Th2, and Th17 cell development 12. BCL6 functions by binding to DNA sequences and recruiting corepressors and histone deacetylases to silence target genes involved in differentiation, apoptosis, and cell cycle control, allowing GC B-cells to tolerate DNA damage from somatic hypermutation and class switch recombination 3. In GC B-cells, BCL6 represses anti-proliferative genes while indirectly promoting pro-GC reactions through microRNA suppression 3. BCL6 dysregulation is clinically significant in hematologic malignancies. BCL6 rearrangements occur frequently in diffuse large B-cell lymphoma (DLBCL) and follicular lymphoma (FL), making BCL6 alterations important diagnostic markers 453. In acute myeloid leukemia (AML), elevated BCL6 maintains leukemia-initiating cell capacity and chemotherapy resistance; BCL6 inhibition reduces AML repopulating cell function without suppressing normal hematopoietic stem cells 6. Additionally, dysregulated BCL6 expression contributes to systemic lupus erythematosus through enhanced Tfh responses 7. BCL6 inhibitors represent a promising therapeutic strategy across multiple malignancies and autoimmune conditions.