SRGAP3 encodes a Rho GTPase-activating protein that primarily inactivates RAC1 to regulate actin cytoskeletal dynamics 1. The protein functions in both cytoplasmic and nuclear compartments, with cytoplasmic SRGAP3 localizing to leading edges via its F-BAR domain to inhibit lamellipodia formation through interaction with lamellipodin 2. Nuclear SRGAP3 interacts with the SWI/SNF chr3 remodeler Brg1 to influence gene expression and dendrite morphology 3. These mechanisms are essential for dendritic spine development and synaptic assembly during neurodevelopment 1. SRGAP3 mutations are associated with intellectual disability in humans 3, and knockout mice exhibit enlarged brain ventricles with ependymal ciliopathy, increased hippocampal volume, and altered behaviors including reduced marble-burying consistent with autism-spectrum phenotypes 4, 5. SRGAP3 is also implicated in neuropathic pain pathogenesis through dendritic spine remodeling 6, and genome-wide association studies identify SRGAP3 as a schizophrenia risk gene 3. Additionally, SRGAP3 shows pleiotropic associations with body fat and Parkinson disease risk 7. Thus, SRGAP3 represents a multifunctional regulator critical for neuronal morphogenesis and neurodevelopmental health.