SEMA3B (semaphorin 3B) is a multifunctional protein with established roles in both developmental and pathological contexts. Developmentally, SEMA3B functions as a chemorepellent that inhibits axonal extension and guides neural development through semaphorin-plexin signaling pathways 1. The protein operates as an extracellular ligand binding to neuropilins and plexins to regulate axon guidance and neural crest cell migration. In disease contexts, SEMA3B operates as a tumor suppressor across multiple cancer types. In lung and renal cancers, SEMA3B suppresses tumor growth through apoptosis induction and angiogenesis inhibition, with promoter and intronic hypermethylation (44-52% and 32-39% respectively) correlating with reduced expression and tumor progression 2. Similarly, in glioma, SEMA3B expression decreases with increasing pathological grade, with methylation-driven silencing in 58% of high-grade tumors 3. In gastric cardia adenocarcinoma, SEMA3B and its antisense lncRNA SEMA3B-AS1 synergistically suppress proliferation, migration, and invasion through Sp1-mediated transcription and interaction with chr3 remodelers 4. Clinically, SEMA3B has recently emerged as a target antigen in membranous nephropathy, a leading cause of nephrotic syndrome in adults 1, 5, 6. SEMA3B-associated membranous nephropathy represents a distinct disease entity with specific clinical and pathologic findings requiring immunohistochemical or mass spectrometry-based detection 5. Additionally, SEMA3B functions as an adipokine in pericoronary epicardial adipose tissue associated with coronary artery disease pathogenesis 7.