SNAP25 is a t-SNARE protein essential for neurotransmitter release through its role in the SNARE fusion machinery 1. As a presynaptic plasma membrane protein, SNAP25 regulates synaptic transmission by controlling both evoked and spontaneous neurotransmitter release 2. Beyond its canonical neuronal function, SNAP25 participates in vesicular trafficking and membrane protein internalization in non-neuronal tissues, including the heart where it regulates atrial potassium channel (Kv1.5) trafficking 3. SNAP25 also promotes fibroblast autophagy through interaction with STX11, suppressing pathological fibroblast activation in pulmonary fibrosis via the PI3K/AKT/mTOR pathway 4. Clinically, SNAP25 mutations cause developmental and epileptic encephalopathies with heterogeneous presentations determined by alterations in spontaneous neurotransmitter release patterns 1. The protein is implicated in multiple neuropsychiatric and neurodegenerative disorders; SNAP25 polymorphisms show significant association with attention-deficit/hyperactivity disorder 56, and SNAP25 deficiency correlates with Alzheimer's and Parkinson's disease pathology 7. SNAP25 protein stability is regulated by TNFAIP1-mediated ubiquitination, and modulating this degradation pathway protects against postoperative cognitive dysfunction 8. These diverse functions establish SNAP25 as a critical regulator of synaptic plasticity and vesicular trafficking with broad therapeutic potential.