GOLT1B (Golgi transport 1B) is a golgi vesicle transporter protein involved in intracellular trafficking. While the precise molecular mechanism remains incompletely characterized, GOLT1B may facilitate fusion of ER-derived transport vesicles with the Golgi complex [UniProt annotation] and plays roles in immune cell differentiation, with dynamic alternative polyadenylation patterns observed during naïve T cell to memory T cell conversion 1. Clinically, GOLT1B has emerged as an oncogenic gene across multiple cancer types. High GOLT1B expression correlates with poor prognosis in most cancers and is primarily driven by copy number amplification 2. In cervical cancer, GOLT1B promotes disease progression by interacting with TANK-binding kinase 1 (TBK1) to activate NF-κB signaling 3, a pathway also implicated in its GO annotations. In breast cancer, GOLT1B upregulation is associated with gene amplification and altered phosphorylation of transcriptional regulators JUN and SIN3A 4. GOLT1B additionally influences the tumor microenvironment through modulation of immune cell infiltration and cancer-associated fibroblasts 24. In colorectal cancer, GOLT1B functions as a downstream target in epithelial-mesenchymal transition pathways 5. Benign 12p12.1p12.2 microdeletions encompassing GOLT1B have been documented with favorable clinical outcomes 6, suggesting haploinsufficiency is generally tolerated.