Autism is a pervasive developmental disorder characterized by impairment in social interaction and communication, and restricted repetitive and stereotyped behavior or interest. Fragile X syndrome and autism have overlapping clinical presentation, thus may share common biochemical and neurophysiological features. Human chromosome 16p11.2 microdeletion is the most common chromosome copy number variation (CNV) in autism. In this study, researchers will generate mice carrying a gene deletion to model human chr16p11.2 microdeletion phenotypes. We hypothesize that this gene deletion will cause synaptic pathophysiology that overlaps with Fragile X syndrome. This hypothesis will be tested in a battery of experiments that have been successfully conducted in Fragile X mice in our laboratory. Identifying the molecular commonalities between autism and Fragile X is vital in understanding the pathogenesis and providing effective therapies for both neurodevelopmental disorders.