SYNGAP1 encodes a synaptic Ras GTPase-activating protein (RASGAP) that functions as a major postsynaptic density constituent essential for synaptic plasticity and neuronal signaling 1. As a dual GTPase-activating protein for Ras and Rap, SYNGAP1 inhibits the Ras-cAMP pathway and integrates into NMDAR signaling complexes, regulating AMPAR membrane trafficking and miniature excitatory postsynaptic currents through mechanisms involving molecular condensate formation rather than solely catalytic activity 2. Beyond synaptic functions, SYNGAP1 is expressed in radial glia cells where it regulates cytoskeletal dynamics critical for cortical neurogenesis 3. De novo SYNGAP1 mutations are among the most frequent genetic causes of autism spectrum disorder and intellectual disability 4, with male-biased enrichment in some populations 5. SYNGAP1 haploinsufficiency causes developmental and epileptic encephalopathy (DEE) characterized by generalized seizures with distinctive eyelid myoclonia, moderate-to-severe intellectual disability, autism spectrum features, and developmental delay 6. Current therapeutic approaches under investigation include splice-switching oligonucleotides to upregulate functional SYNGAP1 isoforms, taurine supplementation, and ketogenic diet intervention 1, though no FDA-approved treatments currently exist for SYNGAP1-related disorders.