PVALB encodes parvalbumin, a calcium-binding protein primarily expressed in fast-spiking GABAergic interneurons throughout the central nervous system. In muscle, parvalbumin facilitates relaxation after contraction by binding two calcium ions 12. In the brain, PVALB+ interneurons form distinct neuronal subtypes critical for neural circuit function. These cells orchestrate social memory through corticothalamic circuits in the thalamic reticular nucleus 3 and regulate cortical network activity including gamma-band oscillations 4. PVALB+ interneurons exhibit selective vulnerability in neurodegenerative and neuropsychiatric diseases. In Alzheimer's disease, loss of PVALB+ inhibitory neurons occurs during advanced disease stages 5, with early synaptic dysfunction involving PVALB dysregulation identified as a disease marker 6. In epilepsy, PVALB+ interneuron subtypes show significant transcriptomic changes and circuit dysfunction 7. Schizophrenia-associated structural variants impair PVALB+ interneuron development, migration, and function 48. Reduced PVALB expression has been documented in autism spectrum disorder and schizophrenia patients 9. Stem cell-derived PVALB+ interneurons successfully differentiate and mature, providing therapeutic potential for drug-resistant epilepsy 10.