BCL9L is a transcriptional coactivator that promotes β-catenin-dependent gene expression and plays a critical role in Wnt/β-catenin signaling 1. The protein contains conserved domains (B9H1-B9H6) that enable binding to β-catenin and interaction with transcriptional machinery, with B9H1 and B9H2 domains functioning as binding regions for Pygo and β-catenin respectively 23. BCL9L mRNA is expressed in multiple tissues including fetal brain, lung, and several tumor types 2. In cancer biology, BCL9L serves as an oncogenic cofactor whose expression is elevated in bladder cancer and associated with tumor progression 45. BCL9L knockdown significantly suppresses cancer cell proliferation, migration, and invasion in bladder cancer models 4. At the mechanistic level, NAT10-mediated acetylation modification regulates BCL9L mRNA stability and translation efficiency in bladder cancer cells 5. Beyond cancer cell-intrinsic effects, BCL9L modulates tumor immunity: targeting BCL9/BCL9L enhances antigen presentation by promoting conventional type 1 dendritic cell activation and infiltration 6, while β-catenin-BCL9/BCL9L signaling suppresses expression of butyrophilin-like molecules, enabling immune evasion from γδ T-cell immunosurveillance in colon cancer 7. These findings position BCL9L as a potential therapeutic target for cancer treatment and immunotherapy.