Abstract: Fragile X syndrome (FXS) is the most common inherited form of intellectual disability and the leading monogenic cause of autism, accounting for 1%–6% of all autism cases in U.S. (Richter et al., 2015; Berry-Kravis et al., 2018; Hagerman and Hagerman, 2022). Patients with FXS exhibit complex and debilitating neurological phenotypes, including impaired cognition and soci a l interactions, hyperactivity, attentional deficits, seizures, sleep disorders, and hypersensitivity (Berry-Kravis et al., 2018; Hagerman and Hagerman, 2022). FXS is caused by an expansion of a CGG trinucleotide repeat within the fragile X messenger ribonucleoprotein 1 (Fmr1) gene, leading to transcriptional silencing of Fmr1 (Berry-Kravis et al., 2018; Hagerman and Hagerman, 2022). Fragile X Messenger Ribonucleoprotein (FMRP), the protein encoded by Fmr1, is an RNAbinding protein that controls the localization, stability, and translation of numerous RNAs essential for synaptic development, plasticity, and architecture (Richter et al., 2015). Decades of research have revealed that loss of FMRP causes synaptic deficits through multiple mechanisms, including exaggerated metabotropic glutamate receptors signaling, elevated translation of synaptic proteins, hypoactivity of inhibitory neurons, dysregulation of presynaptic plasticity, dysfunctional synaptic mitochondria, altered potassium channels, insufficient synaptic elimination, and downregulated autophagy (Berry-Kravis et al., 2018; Yan et al., 2018; Hagerman and Hagerman, 2022; Guo et al., 2023).