Although autism spectrum disorders (ASDs) are highly prevalent, the neural circuitry underlying ASDs remains poorly understood. The cerebellum has been implicated in autism based on human studies, but mouse models that rigorously demonstrate a role for cerebellar dysfunction leading to core features of autism are lacking. Since Tuberous Sclerosis Complex (TSC) is a genetic disorder associated with high rates of comorbid autism, we used conditional knockout mice missing Tsc1 specifically in cerebellar PCs, using L7-Cre deleter line. Homozygous, but not heterozygous, loss of Tsc1 in PCs resulted in increased endoplasmic reticulum stress (as we previously reported for hippocampus1), PC loss, and motor deficits. We found increased dendritic spine density on both heterozygous and homozygous knockout PC dendrites. Interestingly, spine density is reduced in hippocampal neurons with TSC1/2 loss2,3, suggesting diverse mechanisms underlying TSC1/2’s regulation of dendritic spine number in different cell types. Most importantly, both heterozygous and homozygous mutant animals displayed autistic-like behaviors, including abnormal social interaction, repetitive behaviors, and ultrasonic vocalizations, in addition to decreased PC excitability. Treatment of mutants with the mTOR inhibitor, rapamycin, starting at P7 prevented the pathological and behavioral deficits, including the social interaction impairment. Together, these findings implicate the cerebellar PCs in the neural circuitry mediating core features of autism. Since these symptoms are preventable by rapamycin treatment, this mouse model provides an unprecedented opportunity to ask whether critical periods exist for development and treatment of autism-like traits in mice. Therefore, PC-specific Tsc1 mutants have provided us with a valuable experimental system to further investigate the effects of PC dysfunction on the broader neuronal networks and other mechanisms contributing to the pathogenesis of ASDs.