BLNK (B cell linker) is a central adaptor protein that orchestrates B cell receptor (BCR) signaling by bridging the SYK kinase to multiple downstream pathways 1. BLNK is essential for BCR-mediated phospholipase C-gamma (PLC-gamma) activation and calcium mobilization 2, and plays critical roles in activating ERK/MAPK, p38, JNK, NF-κB, and NFAT signaling cascades. It is required for the pro-B to pre-B cell transition and may contribute to BCR-induced B cell apoptosis 1. Beyond B cell function, BLNK unexpectedly regulates innate antifungal immunity by negatively modulating macrophage migration through C-type lectin receptor signaling; BLNK-deficient mice show enhanced resistance to Candida albicans infection 3. Clinically, BLNK deficiency causes autosomal recessive agammaglobulinemia with impaired B cell development 4. BLNK alterations are implicated in Philadelphia chr10-like acute lymphoblastic leukemia, where BLNK activating mutations contribute to aberrant kinase signaling 5. Recent Mendelian randomization studies identified genetically predicted BLNK levels as a causal risk factor for Alzheimer's disease in European ancestry populations 6, and BLNK has been associated with microglial dysfunction in AD pathology 7. Additionally, BLNK expression is dysregulated in chr10 prostatitis, where it modulates inflammatory responses 8.