NAPB (NSF attachment protein beta) is a soluble NSF attachment protein required for vesicular transport between the endoplasmic reticulum and the Golgi apparatus. Mechanistically, NAPB functions in SNARE complex disassembly and synaptic vesicle priming, facilitating intracellular protein transport and synaptic transmission through interaction with synaptobrevin 2-SNAP-25-syntaxin-1a complexes and syntaxin binding. The protein plays critical roles in both constitutive secretory pathway function and regulated synaptic neurotransmission. NAPB mutations are associated with developmental and epileptic encephalopathy 107, highlighting its importance in neurological function. The disease relevance reflects NAPB's essential role in maintaining proper vesicular trafficking and synaptic transmission—processes fundamental to neuronal development and function. Impaired SNARE complex disassembly or synaptic vesicle priming due to NAPB dysfunction would be expected to disrupt neurotransmitter release and cellular protein secretion, potentially explaining the severe neurological phenotype observed in affected patients. Clinically, NAPB represents an important therapeutic target for conditions involving defective vesicular transport or synaptic dysfunction. Understanding NAPB function may inform treatment strategies for developmental and epileptic encephalopathy 107 and potentially other neurological conditions characterized by impaired synaptic transmission or vesicular trafficking defects.