SEPTIN5 is a filament-forming cytoskeletal GTPase that plays critical roles in exocytosis and cellular architecture. In pancreatic β-cells, SEPTIN5 assembles at microtubule-plasma membrane contact sites to anchor insulin secretory granules, and its deletion enhances glucose-stimulated insulin secretion by increasing granule dynamics and access to the plasma membrane, suggesting therapeutic potential for type 2 diabetes 1. In neurons, SEPTIN5 regulates synaptic vesicle exocytosis and undergoes phosphorylation at serine 327 that increases during early Alzheimer's disease pathology, correlating with decreased SEPTIN5 protein levels and affecting amyloid precursor protein processing and autophagy markers 2. SEPTIN5 has been identified as an autoimmune target in rare neurological disorders: antibodies against SEPTIN5 are associated with autoimmune cerebellar ataxia and vestibulocerebellar syndromes, emerging as important diagnostic biomarkers in patients presenting with cerebellar symptoms and ataxia 3, 4. These findings establish SEPTIN5 as a multifunctional protein linking metabolic regulation, neurodegeneration, and autoimmune neurological disease, with potential clinical applications in diabetes management and autoimmune encephalitis diagnosis.